http://www.proteinpower.com/drmike/low-carb-diets/gymnasts-and-low-carb/
Interesting post about anaerobic athletes and a low carb approach.
Friday, February 26, 2010
Wednesday, February 24, 2010
You Can Learn a Lot From a Rat's Eicosanoids
http://wholehealthsource.blogspot.com/2009/05/eicosanoids-fatty-liver-and-insulin.html
This is a fantastic post on an interesting rat chow study - read the whole thing but if you don't have time, here's the conclusion:
"So there you have it folks: direct evidence that insulin resistance, leptin resistance, high blood pressure and fatty liver are mediated by excessive inflammatory eicosanoid signaling. I wrote about something similar before when I reviewed a paper showing that fish oil reverses many of the consequences of a high-vegetable oil, high-sugar diet in rats. I also reviewed two papers showing that in pigs and rats, a high omega-6:3 ratio promotes inflammation (mediated by COX-2) and lipid peroxidation in the heart. Are you going to quench the fire by taking drugs, or by reducing your intake of omega-6 and ensuring an adequate intake of omega-3?
*Of course, they didn't mention the sucrose in the methods section. I had to go digging around for the diet's composition. This is typical of papers on "high-fat diets". They load them up with sugar, and blame everything on the fat. This kind of shenanigans wouldn't fly in a self-respecting field, but it's typical of nutrition-health papers.
**Rats gain fat mass when fed a high-fat diet (even if it's not loaded with sugar), although when the fat is butter or coconut oil, they gain less than if it's vegetable oil. But humans don't gain weight on a high-fat diet (i.e. low-carb diet); to the contrary. What's the difference? It may have to do with the fact that rats eat more calories when they have ad libitum access to high-fat food, while humans don't. In fact, most low-carbohydrate diet trials indicate that participants spontaneously reduce their caloric intake when eating high-fat food."
This is a fantastic post for understanding that no study says only what its author says that the study says. It is the perfect illustration of a 'peer review.'
This is a fantastic post on an interesting rat chow study - read the whole thing but if you don't have time, here's the conclusion:
"So there you have it folks: direct evidence that insulin resistance, leptin resistance, high blood pressure and fatty liver are mediated by excessive inflammatory eicosanoid signaling. I wrote about something similar before when I reviewed a paper showing that fish oil reverses many of the consequences of a high-vegetable oil, high-sugar diet in rats. I also reviewed two papers showing that in pigs and rats, a high omega-6:3 ratio promotes inflammation (mediated by COX-2) and lipid peroxidation in the heart. Are you going to quench the fire by taking drugs, or by reducing your intake of omega-6 and ensuring an adequate intake of omega-3?
*Of course, they didn't mention the sucrose in the methods section. I had to go digging around for the diet's composition. This is typical of papers on "high-fat diets". They load them up with sugar, and blame everything on the fat. This kind of shenanigans wouldn't fly in a self-respecting field, but it's typical of nutrition-health papers.
**Rats gain fat mass when fed a high-fat diet (even if it's not loaded with sugar), although when the fat is butter or coconut oil, they gain less than if it's vegetable oil. But humans don't gain weight on a high-fat diet (i.e. low-carb diet); to the contrary. What's the difference? It may have to do with the fact that rats eat more calories when they have ad libitum access to high-fat food, while humans don't. In fact, most low-carbohydrate diet trials indicate that participants spontaneously reduce their caloric intake when eating high-fat food."
This is a fantastic post for understanding that no study says only what its author says that the study says. It is the perfect illustration of a 'peer review.'
Tuesday, February 23, 2010
HSB Gem on Fructose
http://heartscanblog.blogspot.com/2009/07/goodbye-fructose.html
"A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects. The study is published in its entirety here. Compared to glucose, fructose induced:
1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)
2) 13.9% increase in LDL cholesterol but doubled Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).
3) 44.9% increase in small LDL, compared to 13.3% with glucose.
4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC),fructose increased postprandial triglycerides 99.2%.
The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.
Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.
Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).
Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.
When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says."
Taubes points out in "Good Calories Bad Calories" that part of the negative impact of fructose is that processing it ties up the liver. That means the impact of high blood sugar and subsequent high insulin levels is exacerbated, and therefore insulin resistance is enhanced. Fructose added to a high carb diet is a 'one-two' punch to your metabolism, speeding you on your way to insulin resistance, obesity and metabolic derangement.
"A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects. The study is published in its entirety here. Compared to glucose, fructose induced:
1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)
2) 13.9% increase in LDL cholesterol but doubled Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).
3) 44.9% increase in small LDL, compared to 13.3% with glucose.
4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC),fructose increased postprandial triglycerides 99.2%.
The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.
Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.
Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).
Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.
When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says."
Taubes points out in "Good Calories Bad Calories" that part of the negative impact of fructose is that processing it ties up the liver. That means the impact of high blood sugar and subsequent high insulin levels is exacerbated, and therefore insulin resistance is enhanced. Fructose added to a high carb diet is a 'one-two' punch to your metabolism, speeding you on your way to insulin resistance, obesity and metabolic derangement.
Monday, February 22, 2010
Hijacking Science to Save Us From Ourselves
http://www.time.com/time/health/article/0,8599,1884864,00.html
This a good example of hijacked science.
The facts - people with high blood pressure benefit from reductions in salt intake. If you don't have HBP, there's no evidence to show a BP benefit from reduced salt intake nor an increase in BP from eating too much salt.
These public health models are nice, but they can only make sense as a basis for experimentation. To actually use them as a basis to restrict consumer choices or industry offerings would be madness. Of course, that would not stop the 'true believers' from taking that course ...
This a good example of hijacked science.
The facts - people with high blood pressure benefit from reductions in salt intake. If you don't have HBP, there's no evidence to show a BP benefit from reduced salt intake nor an increase in BP from eating too much salt.
These public health models are nice, but they can only make sense as a basis for experimentation. To actually use them as a basis to restrict consumer choices or industry offerings would be madness. Of course, that would not stop the 'true believers' from taking that course ...
Sunday, February 21, 2010
Amyloid - An Introduction
http://stroke.about.com/od/causesofstroke/a/Amyloid.htm
Gary Taubes highlights this condition as one of the outcomes of chronically high blood sugar levels. BLUF: High sugar levels result it gummy proteins that reduce your body's flexibility, in both interior and external tissues. THink of how problematic that would be for your arteries, for example.
How to avoid amyloid issues? Carb restriction. It frees up your body's 'housekeeping' cells to hunt down and remove the amyloid plaques.
Gary Taubes highlights this condition as one of the outcomes of chronically high blood sugar levels. BLUF: High sugar levels result it gummy proteins that reduce your body's flexibility, in both interior and external tissues. THink of how problematic that would be for your arteries, for example.
How to avoid amyloid issues? Carb restriction. It frees up your body's 'housekeeping' cells to hunt down and remove the amyloid plaques.
Friday, February 19, 2010
More From "Your Unstoppable Heart"
"Those pamphlets adorning your doctor's waiting room may portray LDL as a kind of lone gunman taking a bead on your heart, but they hide a basic fact of science: "Bad cholesterol" is at best a poor shorthand for four major types of independently behaving LDL, each with its own implications for heart disease. We ignore the distinctions at our peril.
Some of these forms of LDL are relatively safe and some are dangerous, and treating them all as one and the same -- the way we do every time we pay our clinic for a three-part lipid panel that simplistically says "LDL: 125" -- is telling us little about the LDL cholesterol that matters, all the while sending health costs through the roof. We may be medicating many people who have no clear need for medication, using drugs that don't target the right particles, and replacing foods that are benign with foods that are anything but.
So in the heart-disease world, we've been stalking the devil we know instead of the devils we don't know. But we need to get to know them if we hope to dodge the number one killer of men.
Some of these forms of LDL are relatively safe and some are dangerous, and treating them all as one and the same -- the way we do every time we pay our clinic for a three-part lipid panel that simplistically says "LDL: 125" -- is telling us little about the LDL cholesterol that matters, all the while sending health costs through the roof. We may be medicating many people who have no clear need for medication, using drugs that don't target the right particles, and replacing foods that are benign with foods that are anything but.
So in the heart-disease world, we've been stalking the devil we know instead of the devils we don't know. But we need to get to know them if we hope to dodge the number one killer of men.
LDL COMES IN FOUR BASIC FORMS: a big, fluffy form known as large LDL, and three increasingly dense forms known as medium, small, and very small LDL. A diet high insaturated fat mainly boosts the numbers of large-LDL particles, while a low-fat diet high in carbohydrates propagates the smaller forms. The big, fluffy particles are largely benign, while the small, dense versions keep lipid-science researchers awake at night.
But here's the problem: The typical LDL test doesn't distinguish between large and small LDL particles -- it can't even spot the difference. And people can have mostly large LDL or mostly small LDL in their overall LDL, depending upon a host of genetic, lifestyle, and environmental factors. Your own personal mix may make all the difference between living to a heart-healthy old age and becoming a Monday-morning casualty at your desk.
Dr. Krauss and collaborators from Harvard and Malmo, Sweden, have helped identify what influences the difference. Working with blood samples from 4,600 healthy Swedish men and women, they used ion mobility analysis to count 11 forms of cholesterol subparticles for each person, and then ran the data through a complex statistical sorting program. After looking for relationships correlating with the 8 percent of people who went on to develop cardiovascular disease, they found three scenarios that predicted it, from the most powerful predictor to the least:
1. High levels of smaller and medium LDL combined with low HDL (a dreaded diabetes-linked syndrome Dr. Krauss had previously called atherogenic lipoprotein phenotype, or pattern B)
2. Low HDL levels
3. High total LDL levels
According to Dr. Krauss, the three risk factors appear to represent three separate processes that put your cardiovascular health at risk. For men, the first two scenarios are more predictive of heart disease, but the third -- high total LDL -- was only marginally predictive of heart disease in men. Nowhere to be seen, of course, is the "total cholesterol" number doctors have been bashing us over the head with for decades. Turns out that number is not as useful a predictor for individuals. "LDL cholesterol is used as a marker for heart-disease risk," Dr. Krauss explains. "It's not a perfect marker, and the particle story is part of the reason for that."
In other words, when you tease apart the subsets of LDL that are preferentially involved in heart disease, total LDL is a less reliable bio-marker. It's like the sniffles that could signal allergies, or the onset of swine flu, or nothing at all. This ambiguity works both ways. Just because you have less of the symptom (statin users take note) doesn't mean you'll have less of the disease. A drop in your total LDL cholesterol might mean nothing at all. A higher LDL cholesterol reading, for that matter, could simply mean you are a healthy person who has learned how to build an amazing sauce out of wine, garlic, shallots, butter, and heavy cream."
But here's the problem: The typical LDL test doesn't distinguish between large and small LDL particles -- it can't even spot the difference. And people can have mostly large LDL or mostly small LDL in their overall LDL, depending upon a host of genetic, lifestyle, and environmental factors. Your own personal mix may make all the difference between living to a heart-healthy old age and becoming a Monday-morning casualty at your desk.
Dr. Krauss and collaborators from Harvard and Malmo, Sweden, have helped identify what influences the difference. Working with blood samples from 4,600 healthy Swedish men and women, they used ion mobility analysis to count 11 forms of cholesterol subparticles for each person, and then ran the data through a complex statistical sorting program. After looking for relationships correlating with the 8 percent of people who went on to develop cardiovascular disease, they found three scenarios that predicted it, from the most powerful predictor to the least:
1. High levels of smaller and medium LDL combined with low HDL (a dreaded diabetes-linked syndrome Dr. Krauss had previously called atherogenic lipoprotein phenotype, or pattern B)
2. Low HDL levels
3. High total LDL levels
According to Dr. Krauss, the three risk factors appear to represent three separate processes that put your cardiovascular health at risk. For men, the first two scenarios are more predictive of heart disease, but the third -- high total LDL -- was only marginally predictive of heart disease in men. Nowhere to be seen, of course, is the "total cholesterol" number doctors have been bashing us over the head with for decades. Turns out that number is not as useful a predictor for individuals. "LDL cholesterol is used as a marker for heart-disease risk," Dr. Krauss explains. "It's not a perfect marker, and the particle story is part of the reason for that."
In other words, when you tease apart the subsets of LDL that are preferentially involved in heart disease, total LDL is a less reliable bio-marker. It's like the sniffles that could signal allergies, or the onset of swine flu, or nothing at all. This ambiguity works both ways. Just because you have less of the symptom (statin users take note) doesn't mean you'll have less of the disease. A drop in your total LDL cholesterol might mean nothing at all. A higher LDL cholesterol reading, for that matter, could simply mean you are a healthy person who has learned how to build an amazing sauce out of wine, garlic, shallots, butter, and heavy cream."
http://www.menshealth.com/men/health/heart-disease/understanding-cholesterol-and-heart-disease/article/34cf5983f7a75210vgnvcm10000030281eac/6#
Thursday, February 18, 2010
Diabetes Linked to Cognitive Decline
"Diabetes can take a toll on the body, taxing the heart, circulation, the kidneys and even the eyes. Now it's becoming clear that the disease may affect the brain as well, contributing to a decline in mental functioning.
Read more: http://www.time.com/time/health/article/0,8599,1869815,00.html#ixzz0eimOiUmG
Studies have shown that diabetes may speed up aging-related deficits in mental function and lead to a twofold increase in the risk of dementia. Some researchers have speculated that diabetes could even boost the risk of developing Alzheimer's disease. Roger Dixon, a psychologist at the University of Alberta in Canada, wanted to learn whether this was true and set out to study exactly how uncontrolled blood sugar affected the brain.
Dixon and his colleagues studied 41 adults with diabetes and 424 healthy adults between the ages of 53 and 90, and reported their findings in the journal Neuropsychology. After testing the participants on memory, recall, verbal fluency, executive functions involving critical thinking and the speed of their mental faculties, researchers found the most significant deficits in diabetes patients on tasks of executive function and speed. These problems showed up in the youngest patients as well as the older ones, and once the cognitive symptoms appeared, they did not seem to worsen or change over time. Although Dixon's study failed to add new information on the question of diabetes and Alzheimer's disease, other experts view these results as useful fodder in the growing field of diabetes research.
"This study in general supports what we understand," says Dr. Alan Jacobson, chief of psychiatric services at the Joslin Diabetes Center in Boston. "It's another study adding to our recognition that Type 2 diabetes portends some type of problem in terms of cognitive function."
Earlier this week, another group of researchers, from Columbia University, reported in the journal Annals of Neurology that spikes in blood-glucose levels affect a region of the brain that forms memories and can lead to faster memory decline in people with diabetes.
Exactly how diabetes is associated with cognitive deficits isn't clear, but there is evidence suggesting that certain areas of the diabetic brain — such as the amygdala, which processes emotions, and the hippocampus, which is related to memory — are smaller than normal, a difference that may affect learning and recall of information. Early studies have even suggested that these physical differences may also predict Alzheimer's disease. While Dixon's study did not find a difference between the diabetes patients and controls on memory skills, Jacobson says the connection between the two diseases is an area of intense research.
As more people develop Type 2 diabetes in adulthood — diabetes has been diagnosed in 20% of American adults, and the vast majority have Type 2 — "more and more people are going to show significant cognitive problems," says Jacobson. "This whole area of research is going to be one of considerable importance in coming years." And studies like this one remind us that conditions like diabetes have wide-ranging effects throughout the body — and that we have only begun to pick apart some of these network connections."
Read more: http://www.time.com/time/health/article/0,8599,1869815,00.html#ixzz0eimOiUmG
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