Redtailblogger

Vitamin B12 Deficiency Can Cause Symptoms That Mimic Aging - NYTimes.com

2011-12-01T10:06:00.000-06:00

Vitamin B12 Deficiency Can Cause Symptoms That Mimic Aging - NYTimes.com

It is an important question. As we age, our ability to absorb B12 from food declines, and often so does our consumption of foods rich in this vitamin. A B12 deficiency can creep up without warning and cause a host of confusing symptoms that are likely to be misdiagnosed or ascribed to aging.

A Vital Nutrient

B12 is an essential vitamin with roles throughout the body. It is needed for the development and maintenance of a healthy nervous system, the production of DNA and formation of red blood cells.

A severe B12 deficiency results in anemia, which can be picked up by an ordinary blood test. But the less dramatic symptoms of a B12 deficiency may include muscle weakness, fatigue, shakiness, unsteady gait, incontinence, low blood pressure, depression and other mood disorders, and cognitive problems like poor memory.

New evidence for a neuronal link between insulin-related diseases and schizophrenia | Observations, Scientific American Blog Network

2011-11-16T11:51:00.000-06:00

New evidence for a neuronal link between insulin-related diseases and schizophrenia | Observations, Scientific American Blog Network

When the body does not properly manage insulin levels, diabetes and other metabolic disorders are familiar outcomes. That hormonal imbalance, however, has also been linked to a higher risk for psychiatric disorders, such as schizophrenia. And a new study has uncovered a potential pathway by which this metabolic hormone can upset the balance of a key neurotransmitter.

"We know that people with diabetes have an increased incidence of mood and other psychiatric disorders," Kevin Niswender, an endocrinologist at Vanderbilt University Medical Center and coauthor of the study, said in a prepared statement. Previous researchers, including Aurelio Galli, a neurobiologist at Vanderbilt, had found that insulin was affecting more than blood sugar levels.

Obesity and energy balance: is the tail wagging the dog?

2011-11-16T11:50:00.000-06:00

European Journal of Clinical Nutrition - Obesity and energy balance: is the tail wagging the dog[quest]

The scientific study of obesity has been dominated throughout the twentieth century by the concept of energy balance. This conceptual approach, based on fundamental thermodynamic principles, states that energy cannot be destroyed, and can only be gained, lost or stored by an organism. Its application in obesity research has emphasised excessive appetite (gluttony), or insufficient physical activity (sloth), as the primary determinants of excess weight gain, reflected in current guidelines for obesity prevention and treatment. This model cannot explain why weight accumulates persistently rather than reaching a plateau, and underplays the effect of variability in dietary constituents on energy and intermediary metabolism. An alternative model emphasises the capacity of fructose and fructose-derived sweeteners (sucrose, high-fructose corn syrup) to perturb cellular metabolism via modification of the adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio, activation of AMP kinase and compensatory mechanisms, which favour adipose tissue accretion and increased appetite while depressing physical activity. This conceptual model implicates chronic hyperinsulinaemia in the presence of a paradoxical state of ‘cellular starvation’ as a key driver of the metabolic modifications inducing chronic weight gain. We combine evidence from in vitro and in vivo experiments to formulate a perspective on obesity aetiology that emphasises metabolic flexibility and dietary composition rather than energy balance. Using this model, we question the direction of causation of reported associations between obesity and sleep duration or childhood growth. Our perspective generates new hypotheses, which can be tested to improve our understanding of the current obesity epidemic, and to identify novel strategies for prevention or treatment.

Does overeating and being lazy make you fat, or do carbs make you overeat and be lazy, as argued by Gary Taubes in Good Calories, Bad Calories?

Low magnesium causes inflammation: Magnesium Research

2011-10-20T22:39:00.000-05:00

Magnesium Research:

To evaluate the association between severe hypomagnesemia and the low-grade inflammatory response in subjects with metabolic syndrome (MetS), ninety-eight individuals with new diagnosis of MetS were enrolled in a cross-sectional study.

-----

Results of this study show that, in subjects with Metabolic Syndrome, severe hypomagnesemia, but not hypomagnesemia, is associated with elevated concentrations of CRP and TNF-α. (inflammation, which can lead to heart disease and other maladies.

Can ghosts help you win the lottery?

2011-10-19T10:35:00.001-05:00

My friend Andy is trying to answer this question on his blog, http://ghostlotto.blogspot.com/. He uses a ghost box, especially tuned to communicate with the other side, and asks the ghosts which lotto numbers will win the lottery that night. He posts videos of the sessions with the ghost box, and info about the lottery as well. Great stuff!http://www.blogger.com/img/blank.gif

Evolutionary Discordance of Grains/Legumes in Diet - PART B

2011-10-19T10:33:00.000-05:00

Evolutionary Discordance of Grains/Legumes in Diet - PART B

Up to this point, we have only briefly touched upon the role cereal grains have in inducing autoimmune disease (except for a brief look at celiac disease). There is substantial evidence (both epidemiological and clinical) showing the role cereal grains may play in the etiology of such diverse autoimmune diseases as multiple sclerosis (MS), insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis, sjogrens syndrome, dermatitis herpetiformis, and IgA nephropathy.

Although this proposal may at first seem preposterous, there is strong data to suggest that cereal grains may be involved in all of these diseases through a process of molecular mimicry whereby certain amino acid sequences within specific polypeptides of the gramineae family are homologous to (have the same structural form as) a variety of amino acid sequences in mammalian tissue. These homologous amino-acid (AA) sequences can ultimately confuse our immune systems so that it becomes difficult to recognize "self" from "non-self." When this happens, T-cells, among other immune-system components, launch an autoimmune attack upon a body tissue with AA sequences similar to that of the dietary antigen.

It seems that grass seeds (gramineae) have evolved these proteins with similarity to mammalian tissue to protect themselves from predation by mammals, vertebrates, and even insects. This evolutionary strategy of molecular mimicry to deter predation or to exploit another organism has apparently been with us for hundreds of millions of years and is a quite common evolutionary strategy for viruses and bacteria. It has only been realized since about the mid-1980s [Oldstone 1987] that viruses and bacteria are quite likely to be involved in autoimmune diseases through the process of molecular mimicry. Our research group has put together a review paper compiling the evidence (and the evidence is extensive) implicating cereal grains in the autoimmune process, and with a little bit of luck it should be published during 1998. [Editorial note as of June 1999: The paper has now been published; the citation is: Cordain L (1999) "Cereal grains: humanity's double-edged sword." World Review of Nutrition and Dietetics, vol. 84, pp. 19-73.]

Without the evolutionary template and without the evidence provided us by the anthropological community showing that cereal grains were not part of the human dietary experience, the idea that cereal grains had anything to do with autoimmune disease would probably have never occurred to us. This new electronic medium has allowed instant cross-fertilization of disciplines which probably would have rarely occurred as recently as five years ago.

A fresh approach - Diet for autistics - brisbanetimes.com.au

2011-10-19T10:32:00.000-05:00

A fresh approach - Diet - Life & Style Home - brisbanetimes.com.au:

Simply put, the rationale is that, to differing degrees, children lack the intestinal bacteria (perhaps due to hereditary factors, perhaps antibiotics, perhaps both) and enzymes needed to digest food, absorb nutrients and eliminate toxins, particularly casein and gluten, which break down in the gut into compounds with "opiate agonist" (or drug-like) properties.

Children with autism are said to have "abnormal leakage" from the gut, allowing these substances to pass into the central nervous system and disrupt brain function - in effect fog up the brain, because they mimic the effects of endorphins.

The "cellular malnutrition" throughout the body that also results from this gut dysfunction in a child is exacerbated if the diet includes processed food with additives, preservatives, emulsifiers and too much sugar.

Why the Low Carb Diet is Best - Diabetes Health

2011-10-19T10:31:00.000-05:00

Why the Low Carb Diet is Best - Diabetes Health

Virtually the entire evolution of mankind occurred when our ancestors were hunter-gatherers, well before the inventions of agriculture and animal husbandry. (2) These people had scarcely any access to dietary carbohydrate and certainly no access to animal milk, cereal grains, whole-grain and refined breads, refined sugars, and sweet fruits. They ate almost exclusively lean meat and fish, plus small amounts of leafy and other low carbohydrate vegetables. Some humans, such as Eskimos, consumed only fat and protein. Our pre-agriculture ancestors frequently had violent deaths, but no coronary, kidney, or arterial disease, no tooth decay, and no diabetes.

By 1969, when I first began to measure my own blood sugars, I was already suffering from about 15 major and minor long-term complications of diabetes, thanks to the low fat, high carbohydrate diet I had been following for 23 years. By about this time, scientific studies of animals had demonstrated the prevention and even reversal of many diabetic complications by blood sugar normalization.

I soon discovered that even multiple daily insulin injections (basal/bolus dosing) would not achieve anything close to steady normal blood sugars. It was not until I lowered my carbohydrate consumption to a daily total of 30 grams (mostly from leafy and cruciferous vegetables) that things fell into place. Today my A1c is 4.5% (normal is 4.2-4.6%), and my target blood sugar is 83 mg/dl (about mid-normal for young non-diabetic adults).

Wheat Belly- interesting new book is out

2011-10-19T10:29:00.002-05:00

Wheat Belly -- The Toll of Hubris on Human Health

Dr. William Davis, Milwaukee-based "preventive cardiologist" and Medical Director ohttp://www.blogger.com/img/blank.giff the Track Your Plaque program, argues in his new book, Wheat Belly: Lose the Wheat, Lose the Weight, and Find Your Path Back to Health, that "somewhere along the way during wheat's history, perhaps five thousand years ago but more likely fifty years ago, wheat changed." And not for the better.

William Davis, MD, hosted at The Wheat Belly Blog

According to Dr. Davis, the introduction of mutant, high-yield dwarf wheat in the 1960s and the misguided national crusade against fat and cholesterol that caught steam in the 1980s have conspired together as a disastrous duo to produce an epidemic of obesity and heart disease, leaving not even the contours of our skin or the hairs on our heads untouched. Indeed, Dr. Davis argues, this mutant monster we call wheat is day by day acidifying our bones, crinkling our skin, turning our blood vessels into sugar cubes, turning our faces into bagels, and turning our brains into mush.

Dr. Davis's central thesis is that modern wheat is uniquely able to spike our blood sugar with its high-glycemic carbohydrate and to stimulate our appetite with the drug-like digestive byproducts of its gluten proteins. As a result, we get fat. And not just any fat — belly fat. "I'd go so far as saying," he writes, "that overly enthusiastic wheat consumption is the main cause of the obesity and diabetes crisis in the United States" (p. 56, his italics). Abdominal obesity brings home a host of inflammatory factors to roost, causing insulin resistance and the production of small, dense LDL particles prone to oxidation and glycation. The high blood sugar and insulin levels further contribute to acne, hair loss, and the formation of advanced glycation endproducts (AGEs) that accelerate the aging process.

She Rocks

2011-09-01T00:17:00.001-05:00

New video from Armen Moradians!
Spaceship of the imagination

Rethinking the Atkins diet

2011-08-29T11:56:00.000-05:00

In diet studies, big question goes unexplored
My Turnhttp://www.blogger.com/img/blank.gif

August 23, 2010|By Bob Kaplan, Special to the Los Angeles Times

After losing weight and keeping it off on the Atkins diet, it seems odd that no one wants to find out why this higher-calorie option appears to be more effective.

Researchers (funded by the National Institutes of Health) randomized half their subjects to a diet that limited both calories and fat — women ate no more than 1,500 calories a day; men no more than 1,800. The other half were told to avoid carbohydrate-rich foods, as I've been doing for 15 years, but could eat all the protein and fat they wanted.

The study's authors concluded both diets were equally effective for weight loss, and that is how the press reported it. But the low-carb diet also was associated with better heart health.

Let that sink in for a moment.

The people on the low-fat, low-calorie diet were enduring what nutritionists used to call "semi-starvation diets." They were presumably being deprived of the pleasure of satiation and expected to go at least a little bit hungry every day. Yet the diet that allowed for gluttony was just as effective, and healthier, than the diet that implied temperance, moderation and self-restraint.

The study raises two important questions about our national problems with weight: First, why would a diet unrestricted in calories produce the same amount of weight loss as a diet that requires, in effect, a lifetime of semi-starvation and the one we've been told to live by throughout the obesity epidemic: eat fruits and vegetables and whole grains and low-fat dairy products, just eat significantly less of them?

Can a High-Fat Diet Beat Cancer? Time Magazine

2011-08-29T11:54:00.001-05:00

Can a High-Fat Diet Beat Cancer?
By Richard Friebe
http://www.blogger.com/img/blank.gif
The theory is simple: If most aggressive cancers rely on the fermentation of sugar for growing and dividing, then take away the sugar and they should stop spreading. Meanwhile, normal body and brain cells should be able to handle the sugar starvation; they can switch to generating energy from fatty molecules called ketone bodies — the body's main source of energy on a fat-rich diet — an ability that some or most fast-growing and invasive cancers seem to lack.

The Würzburg trial, funded by the Otzberg, Germany–based diet food company Tavartis, which supplies the researchers with food packages, is still in its early, difficult stages. "One big problem we have," says Schmidt, sitting uncomfortably on a small, wooden chair in the crammed tea kitchen of Kämmerer's lab, "is that we are only allowed to enroll patients who have completely run out of all other therapeutic options." That means that most people in the study are faring very badly to begin with. All have exhausted traditional treatments, such as surgery, radiation and chemo, and even some alternative ones like hyperthermia and autohemotherapy. Patients in the study have pancreatic tumors and aggressive brain tumors called glioblastomas, among other cancers; participants are recruited primarily because their tumors show high glucose metabolism in PET scans.

Four of the patients were so ill, they died within the first week of the study. Others, says Schmidt, dropped out because they found it hard to stick to the no-sweets diet: "We didn't expect this to be such a big problem, but a considerable number of patients left the study because they were unable or unwilling to renounce soft drinks, chocolate and so on."

The good news is that for five patients who were able to endure three months of carb-free eating, the results were positive: the patients stayed alive, their physical condition stabilized or improved and their tumors slowed or stopped growing, or shrunk. These early findings have elicited "very positive reactions and an increased interest from colleagues," Kämmerer says, while cautioning that the results are preliminary and that the study was not designed to test efficacy, but to identify side effects and determine the safety of the diet-based approach.

Read more: http://www.time.com/time/health/article/0,8599,1662484,00.html#ixzz1WRCqBaYh

Low-salt diet increases insulin resistance in healthy subjects

2011-08-29T11:51:00.002-05:00

Low-salt diet increases insulin resistance in healthy subjects

Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.http://www.blogger.com/img/blank.gif

Eat your salt without fear!

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet

2011-08-26T12:45:00.000-05:00

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet

Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications
for rising health care costs. Huge amounts of research money are currently being http://www.blogger.com/img/blank.gifinvested in seeking the
underlying cause, with corresponding progress in understanding the disease progression. In this paper, we
highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in
dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the
pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins
concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which
significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate
signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial
infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with
Alzheimer's disease, and may also be due in large part to this same underlying cause.
© 2011 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.

Comparing Effects of a Low-energy Diet and a High-protein Low-fat Diet on Sexual and Endothelial Function, Urinary Tract Symptoms, and Inflammation

2011-08-26T12:39:00.001-05:00

Comparing Effects of a Low-energy Diet and a High-protein Low-fat Diet on Sexual and Endothelial Function, Urinary Tract Symptoms, and Inflammation in Obese Diabetic Men

Introduction. Abdominal obesity and type 2 diabetes mellitus are associated with sexual and endothelial dysfunction, lower urinary tract symptoms (LUTS), and chronic systemic inflammation.

Conclusions. Diet-induced weight loss induces rapid improvement of sexual, urinary, and endothelial function in obese diabetic men. A high-protein, carbohydrate-reduced, low-fat diet also reduces systemic inflammation and sustains these beneficial effects to 1 year.

Effect of short-term low- and high-fat diets on low-density lipoprotein particle size in normolipidemic subjects

2011-08-26T12:35:00.001-05:00

http://www.sciencedirect.com/science/article/pii/S0026049511001764
http://www.blogger.com/img/blank.gif

The high-fat diet was also associated with a significant increase in LDL particle size (255.0 vs 255.9 Å; P = .01) and a significant decrease in the proportion of small LDL particle (<255.0 Å) (50.7% vs 44.6%, P = .01). As compared with a low-fat diet, the cholesterol-raising effect of a high-fat diet is associated with the formation of large LDL particles after only 3 days of feeding.

(larger particles are much healthier for you, and come about after only days on a low carb diet)

Remission of diabetes in a week using low carb

2011-08-20T14:30:00.001-05:00

http://resources.metapress.com/pdf-preview.axd?code=16721831571j7360&size=largesthttp://www.blogger.com/img/blank.gif

Low calorie, low carb diet leads to remission of type 2 diabetes within a week.

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet

2011-06-01T18:44:00.000-05:00

ScienceDirect - European Journal of Internal Medicine : Nutrition and Alzheimers disease: The detrimental role of a high carbohydrate diet

Abstract

Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause.

Keywords: Advanced glycation end-products; Alzheimer's disease; Cholesterol

- Add lithium to the water supply? WWW.THEDAILY.COM

2011-05-25T16:10:00.000-05:00

- WWW.THEDAILY.COM Interesting article that says some scientists would like to add lithium to the water supply to decrease suicides and violence, make us all happier.

Eating less salt doesn't cut heart risks: study - Yahoo! News

2011-05-04T12:17:00.000-05:00

Eating less salt doesn't cut heart risks: study - Yahoo! News:

"NEW YORK (Reuters Health) – People who ate lots of salt were not more likely to get high blood pressure, and were less likely to die of heart disease than those with a low salt intake, in a new European study.

The findings 'certainly do not support the current recommendation to lower salt intake in the general population,' study author Dr. Jan Staessen, of the University of Leuven in Belgium, told Reuters Health."

Scientists now saying carbs, not fat, are to blame for America's ills - latimes.com

2010-12-19T10:53:00.000-06:00

Scientists now saying carbs, not fat, are to blame for America's ills - latimes.com

Most people can count calories. Many have a clue about where fat lurks in their diets. However, fewer give carbohydrates much thought, or know why they should.

But a growing number of top nutritional scientists blame excessive carbohydrates — not fat — for America's ills. They say cutting carbohydrates is the key to reversing obesity, heart disease, Type 2 diabetes and hypertension.

"Fat is not the problem," says Dr. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health. "If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks, we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases."

It's a confusing message. For years we've been fed the line that eating fat would make us fat and lead to chronic illnesses. "Dietary fat used to be public enemy No. 1," says Dr. Edward Saltzman, associate professor of nutrition and medicine at Tufts University. "Now a growing and convincing body of science is pointing the finger at carbs, especially those containing refined flour and sugar."

Gastrointestinal transit, post-prandial lipaemia and satiety following 3 days high-fat diet in men

2010-12-19T10:00:00.000-06:00

European Journal of Clinical Nutrition - Abstract of article: Gastrointestinal transit, post-prandial lipaemia and satiety following 3 days high-fat diet in men

Background/Objectives:

High-fat (HF) diets of 2 weeks have been shown to accelerate gastric emptying (GE). To date, no studies have shown any alteration in GE following shorter HF diets. The aim of this study was to assess if an HF, high-energy diet of 3 days can adapt gastrointestinal (GI) transit, blood lipids and satiety.
Subjects/Methods:

Eleven male volunteers participated in a study consisting of three, 3-day interventions each separated by a test day. During the first intervention, volunteers recorded their diet. In the second and third interventions, volunteers repeated their food diary plus either a low-fat yogurt or HF yogurt supplement in randomized order. Test days involved measurement of GE using the 13C octanoic-acid breath-test, mouth-to-caecum transit time (MCTT) using the inulin H2 breath test and satiety using visual analogue scales. Blood samples for measurement of lipaemia were taken using a venous cannula.
Results:

MCTT was different between the three test days (P=0.038), with the shortest MCTT following the HF intervention. GE was shortest following the HF intervention. There were no differences in satiety between the interventions. The High Fat intervention reduced triglycerides, total cholesterol and low-density lipoprotein cholesterol, and increased high-density lipoprotein cholesterol.
Conclusion:

This study shows that changes in GI transit owing to an HF diet can occur in a time period as short as 3 days.

cardiovascular risk factors linked to frontal lobe glucose metabolism

2010-11-20T01:26:00.000-06:00

An inverse association of cardiovascular risk and frontal lobe glucose metabolism

Neurology. 2009 February 24; 72(8): 738–743.
doi: 10.1212/01.wnl.0000343005.35498.e5.

PMCID: PMC2677543
Copyright © 2009 by AAN Enterprises, Inc.
An inverse association of cardiovascular risk and frontal lobe glucose metabolism
B Kuczynski, PhD, W Jagust, MD, H C. Chui, MD, and B Reed, PhD
From the Helen Wills Neuroscience Institute, University of California, Berkeley, and the Lawrence Berkeley National Laboratory (B.K., W.J.); the Department of Neurology (H.C.C.), University of Southern California, Los Angeles; and University of California, Davis, Alzheimer’s Center and Northern California Veterans Affairs Health Care System (B.R.).

Abstract
Objective:
To investigate associations between vascular risk profile and cerebral glucose metabolism.
Methods:
Subjects ranged from normal to having dementia (age >55 years) and underwent neuropsychological testing, MRI, and FDG PET scanning (n = 58). The Framingham Cardiovascular Risk Profile (FCRP) and its individual components were used as covariates in regression analyses with each PET scan using SPM2.
Results:
Analyses revealed broad areas of the frontal lobe in which higher FCRP was associated with lower normalized glucose metabolism including the superior medial frontal, superior frontal and superior orbital frontal cortex and the ventrolateral prefrontal cortex. Significant associations were predominately found in the left hemisphere. Independent component analyses revealed interesting regions but further confirm the relevance of the integrative measure of coronary risk.
Conclusions:
Although the mechanism of this association bears further investigation, this finding provides further evidence that vascular risk factors have malignant effects on the brain, particularly in the prefrontal cortex.

Frontal lobe dysfunction is associated with attention deficit disorder. Not mentioned here, but these cardiac risk factors are also associated with depression, a condition known as vascular depression.

Paleo expert Melissa McEwen interviewed on her conversion from veganism

2010-11-19T17:50:00.002-06:00

Let Them Eat Meat : Interview With an Ex-Vegan: Melissa McEwen

Interview With an Ex-Vegan: Melissa McEwen

Unless you’ve been living in a cave for the past few months, you probably read “New Age Caveman in the City,” the New York Times feature on aspiring Stone Agers in NYC. If so, you may remember Melissa McEwen as the lone cavewoman of the group, providing some refreshing gender balance to the paleo diet argument that rice cakes and rolled oats aren’t health foods — meat is.

Melissa discusses the paleo diet and all its meaty nutrients on her site Hunt.Gather.Love, on Twitter and sometimes in the comments of the blog you’re reading right now. On top of that, she’s scheduled to speak at the Ancestral Health Symposium in Los Angeles next summer and she’s just been interviewed by Let Them Eat Meat. You might say that Melissa is already a star in the paleo world.

But of course none of this would have been possible if Melissa had stuck with veganism.

Melissa holds building together

What’s all this about animal foods being nutritious? Didn’t you used to be vegan?

I’ve always had terrible health problems: stomach issues, migraines and allergies were the worst ones. I assumed it was because of my picky eating habits. Whenever I felt sick my mother would tell me it was because I didn’t eat enough vegetables. Then when I got to college I was diagnosed with gastroesophageal reflux disease and irritable bowel syndrome.

I read John Robbins’ Diet for a New America, which talked about how many common health ailments were related to diet, particularly animal products. I lived in a dormitory that had a vegetarian cafeteria and started eating there. A few things got better, but I still was on many medications. At one point I think I was on 13 different ones!

I was involved in several environmental groups and met many vegans that I admired. They convinced me that veganism was more logical than vegetarianism, since milk and eggs involve plenty of dead animals, so I cut those out too.

But I still didn’t feel great. When I moved into a dorm without a cafeteria I started experimenting with my diet. I did a pretty lengthy elimination diet and realized gluten was the probable cause of my GERD, but that other grains seemed to irritate my digestive system as well.

Did you try cutting out grains?

I did grain-free veganism for several months, but I struggled with chronic hunger. I would lapse by eating cheese at some public function and then feel gross and guilty. I ate at the local vegan restaurant, The Red Herring, as often as possible. But whenever I ate there I got sick.

Then I got really sick. It took my doctors some time to figure out what I had because they weren’t sure if my other illnesses had gotten worse or if I had a new illness. It turns out I had salmonella and that it had taken up residence. Most young people are able to clear salmonella within a few days, but it had tormented me for over a month. I had to go on some heavy duty antibiotics.

I fell into raw veganism because my digestive system was trashed and I thought maybe it would be the cure. So many people on raw vegan boards have stories about how it’s such a wonderful diet and because of it they are no longer sick. I believed them. I definitely felt much better… at first.

This is the common lament of raw veganism. It eliminates most problematic foods, but where is the nutrition? At this point I had been sick enough that I just wanted to get better and after reading Art De Vany’s writings on evolutionary diet and fitness, I decided to follow his recommendations.

[...]

What was your major?

I studied agricultural economics at the University of Illinois and then forest ecology at the Swedish University of Agriculture. I kept waffling between majors and so I took a diverse selection of courses — food/agricultural law, nutrition science, econometrics, environmental economics, entomology, development economics, toxicology, crop science and anthropology.

I plan on eventually doing a PhD in forestry or natural resource economics and I would also like to have my own farm.

Fantastic article with a very smart lady! Melissa's blog Hunt, Gather, Love is excellent, and in this article she talks about her journey to paleo from veganism, and displays a deep knowledge of nutrition and dietary issues. I did the vegetarian thing for a few years after reading John Robbins’ Diet for a New America as well, and gained a ton of weight, weight which I struggled to lose. I went off vegetarianism after reading the book The Paleolithic Prescription, which was fascinating, and disabused me of my vegetarian philosophy.

The Case For Going Gluten Free Medical Journal References | Evolvify

2010-11-19T17:37:00.001-06:00

The Case For Going Gluten Free Medical Journal References | Evolvify

In the U.S., public awareness of gluten free diets has reached widespread recognition, but largely in name only. For those suffering with celiac disease or acute wheat allergies, it’s critical. For those with known reactions to gluten, it’s of serious importance. For those who don’t really know what it’s about, but see it on packaging, it seems to evoke a similar response as being forced to “Press 1 for English”. Journalists tend to frame the gluten free approach as legit for celiac treatment, but ultimately a fad diet controlling minions of mindless Gwyneth Paltrow lovers (AP Article). The paleo diet community views it as more of a religion (that’s tongue-in-cheek hyperbole, people!). Before we continue, here are my biases: I experience repeatable, specific, and boring symptoms from gluten intake, but I do not have celiac disease or a “gluten allergy”. Evolutionary biology is a scientific fact and I believe the paleo diet provides ultimate explanations for why we should’t eat grains. So what are the proximate explanations for going gluten free? Is it fad or fo’ real?
A quick and dirty primer

Celiac (or coeliac) disease is an autoimmune disorder in which the small intestine is damaged by components of gluten, a protein found in wheat and other grains. The effects of celiac diseas are numerous, serious, and varied. For a entertaining sobering look, check out Tim Ferriss’ How to Keep Feces Out of Your Bloodstream. Strictly speaking, a “wheat allergy” can be similar to something like a peanut allergy. Folks in this group experience rapid onset symptoms that are serious, including the potential of anaphylactic shock. It’s mainly for these folks that food is required to expose the presence of wheat content on packaging.

From there, we transition into the murky terms of gluten intolerance and/or sensitivity. These two classifications are where the non-celiac, non-allergy folks may reside. Whether we should take them seriously is what the references below try to answer. There’s plenty of research and anecdotal evidence within the paleo and related nutrition/health worlds. However, since they’re in it for the money, some people tend to pass what they say off as mere profiteering. And perhaps that’s fair, but perhaps both are justified.

Below are a series of links (and abstracts when available) to recent medical literature on gluten research. Basically, I just did a search on PubMed for articles with “gluten” in the title, but without “celiac” or “coeliac” in the title. Doing this search brought up 1340+ results, so I narrowed it down. I’ve tried to filter out the articles discussing the use of gluten free diets in the treatment of autism. I’ve also endeavored to filter out everything relating to animal studies. That said, some of the animal studies are quite convincing… But I get it… Humans aren’t chimpanzees or mice. Also, I only went back to 2008 (this was written in September, 2010).

[...]

Current Barometer

My assessment of the current barometer for medical research on the effect of gluten on humans is roughly this: In the general population (those not having celiac disease or wheat allergies), gluten either causes, or is strongly correlated to a range of autoimmune and neurological disorders. Further, gluten intolerance can present with any one, or group, of symptoms or disorders with varying degrees of severity. Lastly, it is generally agreed that celiac disease and non-celiac gluten intolerance are underreported and under-diagnosed, though the numbers remain speculative.

For me, on a practical level, the correlations between autoimmune and neurological problems in the scientific literature, my personal experiences with gluten, anecdotal reports from others, and the logical framework of evolutionary biology/paleo diet is convincing enough for me to abstain from gluten.

Andrew brings together a ton of great links to research studies showing the negative effects of gluten in this post on his blog, evolvify.com. I see many of these studies show the gluten link to schizophrenia, as seen in my last blog post below. Learning about celiac was a real revalation to me that started me on my own low carb journey. How can carbs be so essential to human health if a segment of the population is allergic to them? That's not how evolution works at all.

Dietary Sugar and Mental Illness: A Surprising Link | Psychology Today

2010-11-19T17:30:00.001-06:00

Dietary Sugar and Mental Illness: A Surprising Link | Psychology Today

Dietary Sugar and Mental Illness: A Surprising Link
Sugar and Mental Illness: A Surprising Link
Published on July 23, 2009

Noted British psychiatric researcher Malcolm Peet has conducted a provocative cross-cultural analysis of the relationship between diet and mental illness. His primary finding may surprise you: a strong link between high sugar consumption and the risk of both depression and schizophrenia.

In fact, there are two potential mechanisms through which refined sugar intake could exert a toxic effect on mental health.

First, sugar actually suppresses activity of a key growth hormone in the brain called BDNF. This hormone promotes the health and maintenance of neurons in the brain, and it plays a vital role in memory function by triggering the growth of new connections between neurons. BDNF levels are critically low in both depression and schizophrenia, which explains why both syndromes often lead to shrinkage of key brain regions over time (yes, chronic depression actually leads to brain damage). There's also evidence from animal models that low BDNF can trigger depression.

Second, sugar consumption triggers a cascade of chemical reactions in the body that promote chronic inflammation. Now, under certain circumstances (like when your body needs to heal a bug bite), a little inflammation can be a good thing, since it can increase immune activity and blood flow to a wound. But in the long term, inflammation is a big problem. It disrupts the normal functioning of the immune system, and wreaks havoc on the brain.

Inflammation is associated with an increased risk of heart disease, diabetes, arthritis, and even some forms of cancer . . . it's also linked to a greater risk of depression and schizophrenia. And again, eating refined sugar triggers inflammation. So does eating heavily processed molecular cousins like 'high fructose corn syrup'.

Not surprising to me, ha ha! I've seen a good amount of evidence for this. Something as simple as sugar can have so many different effects in different people. It may be hard for people to believe that my obesity, Fred's depression, Mary's arthritis, and Joe's schizophrenia can all be traced to refined carbs, but the evidence is there. I read some interesting stuff a while back about "insulin shock" therapy. They gave people hyperdoses of insulin, putting them into a diabetic coma. Then later they would wake them up with a glucose injection. Sometimes it worked. One of the most famous people treated was physicist John Nash, portrayed by Russell Crowe in the movie A Beautiful Mind. Seems to me as if there's a connection between the insulin/sugar process and schizophrenia for some people. There's also evidence that cannabis use in susceptible users may encourage the development of schizophrenia. I'm not sure how solid that link is, and if it's based on simple correlation observed in epidemiological studies, which would not necessarily imply causation. But if there is a link, I wonder about the fact that some report that using cannibis can affect blood sugar, I believe by lowering it acutely, leading to the munchies. Speculation, but again, I like looking for links.

Epilepsy’s Big, Fat Miracle - Ketogenic diet as treatment

2010-11-19T17:18:00.001-06:00

Epilepsy’s Big, Fat Miracle - NYTimes.com

Starvation had long been one approach to treating epilepsy. Deny the patient food for, say, a week and often their seizures went away. But there were obvious limits on how long starvation could be used as a treatment. In the 1920s, researchers at the Mayo Clinic, looking for a way to treat diabetics, figured out that it was not fasting per se that helped control seizures. Rather, they found that it was what the body did during an extended fast that helped control them. Deprived of food, the human body starts burning body fat as fuel, and it was that process of ketosis that somehow had the antiepileptic effect. Trick the body into thinking it was starving by taking away its primary fuel of carbohydrates and forcing it to subsist on an all-fat diet, and you could create that antiepileptic effect as long as necessary.

The diet was quickly adopted and widely used through the 1930s. And then, almost as fast as it had appeared, the keto diet disappeared. When Dilantin was first used as an antiepileptic drug in 1938, its success steered medical minds toward pharmaceutical solutions. A generation later, the diet had been all but forgotten. There was no scientific evidence that it worked, after all. More important, it was incredibly difficult to administer. Even in the 1990s, Millicent Kelly, Charlie Abrahams’s dietitian at Johns Hopkins, was planning menus with a calculator and a legal pad.

By 2000, more people were asking about keto, but most pediatric neurologists still would not prescribe it. That bias seemed ridiculous to J. Helen Cross, the principal investigator of the 2008 randomized keto trial at University College London. “I’d been dealing with complex epilepsy cases for 10 years, and it was quite clear to me that certain children did respond to the ketogenic diet,” Cross says. “But we in our institution — and I know we weren’t alone — were coming up against barriers to get the resources to do it. They’d say there’s no evidence it works. It’s a quack diet. There is no controlled data. So I wanted to prove that it did work once and for all, and do it in a way so that people couldn’t argue with it.”

It took five years to enroll and track enough patients to make the study credible and another two years to analyze the data and undergo the rigorous academic peer-review process. But since the study was published in 2008, it has answered doubts about keto’s clinical effectiveness.

Keto has now attracted attention from all corners of the neurological community. Two scientists at the National Institutes of Health are planning a study of its effectiveness in Parkinson’s patients. Papers published in the past two years suggest that keto may slow the growth of a brain tumor in mice. A biotechnology company named Accera is marketing a high-fat powder to Alzheimer’s patients that is supposed to reproduce the effects of ketosis, without the dietary restrictions of keto.

Still, there is one giant unanswered question: Why does keto work? Jong Rho, the head of pediatric neurology at the University of Calgary and the Alberta Children’s Hospital, theorizes that ketone bodies — the compounds made by the liver when the body burns fat for energy — protect brain cells from being damaged. Rho, who just received a $2 million, five-year grant from the National Institutes of Health to continue to investigate this theory, says experiments with epileptic mice suggest that extended time on the diet makes them more seizure-resistant.

Rho’s theory, however, only raises more questions. How would ketone bodies protect brain cells? Scientists don’t have a clue about how our cells react during ketosis. They don’t even know how much ketone bodies themselves matter. Until scientists understand the basic biological mechanisms, they can’t begin to embark on the long and costly process of drug development.

The success of the pediatric diet seems to have made it easier for keto scientists to get money for this basic research. “Before Helen’s study, we all had a clear sense that keto worked,” says Carl Stafstrom, the head of pediatric neurology at the University of Wisconsin, “but we couldn’t say in a grant proposal that the diet has been proven to be effective. Now we can.” There are recently financed studies, for example, exploring why the body resists ketosis and exploring compounds that might trigger the antiepileptic mechanism.

[...]

There has been so much buzz around keto that neurologists and scientists have begun wondering what else it can do. Could it be used to treat seizures in adults? What about Parkinson’s, Alzheimer’s, A.L.S. and certain cancers? Tumors typically need glucose to grow. There is very little of this simple sugar in a keto diet, and there have been interesting results with mice that suggest the diet might slow tumor growth. These scientific explorations are in their early stages and may not amount to much. Nonetheless, researchers are taking them seriously.

Fantastic article on the ketogenic diet for the treatment of epilepsy.

Treatment zaps high blood pressure at the source

2010-11-19T17:08:00.002-06:00

Treatment zaps high blood pressure at the source

By Julie Steenhuysen Julie Steenhuysen – Wed Nov 17, 12:18 pm ET

CHICAGO (Reuters) – A device that destroys nerves leading to the kidney safely lowered blood pressure in people with treatment-resistant hypertension, potentially offering a new option for millions of people who struggle to keep their disease in check, researchers said on Wednesday.

The device, made by privately held Ardian Inc of Mountain View, California, lowered the top blood pressure reading by an average of 32 points after six months, compared with no change in patients who took the best available medicines.

"There are a lot of questions, but it is very exciting," said Dr. Suzanne Oparil of the University of Alabama at Birmingham, who reviewed the findings presented at the American Heart Association meeting in Chicago.

The one-time treatment works by silencing nerves leading into and out of the kidney, which play a central role in the sympathetic nervous system, the body's "fight or flight" response that can increase heart rate and blood pressure.

Procedures that surgically disrupt these nerves had been shown to lower high blood pressure decades ago, but were abandoned with the advent of drugs that target the renin-angiotensin system, which regulates blood pressure and fluid retention.

"Those drugs are good but not perfect," said Dr Murray Esler of the Baker IDI Heart and Diabetes Institute in Melbourne, Australia, whose findings were released online by the Lancet.

"We can see that because of their failure in the patients on this trial. They are all on drugs of this type."

BLOOD PRESSURE READING FELL BY 32 POINTS

High blood pressure, or too much force exerted by blood as it moves against vessel walls, is the leading risk factor for premature death worldwide.

Nearly half of Europeans have hypertension, and in the United States, about 75 million Americans do -- and only two-thirds of those people are treated. Among those who are, half do not get their blood pressure under control.

Normal blood pressure is considered to be 120 over 80 or lower. A top reading of over 140 is considered high blood pressure.

[...]

After six months, blood pressure among those who got the treatment fell by 32 points on the top reading and 12 points on the bottom reading, pushing some into the near-normal range. There was no change in the control group.

"It was a big effect," Esler said. "The main pressure in the group after denervation was 145, and in 39 percent of them, it was 140 systolic."

"It's a much bigger effect than you would anticipate in a drug trial, particularly in these people, who are resistant to drugs anyway," Esler said.

Very, very interesting. Especially the part about the kidneys and the sympathetic nervous system being a controlling element of hypertension. I was able to dig up other info on the kidney-hypertension link, and it's pretty solid. Low carb and/or fasting is a more natural treatment option. The low carb route also helps the other parts of metabolic syndrome (low HDL, high Triglcyerides, abdominal obesity, high blood sugar, and hypertension), whereas this treatment only affects one. I'm curious why it doesn't seem to affect the other factors, and also wonder if it has any effect on mortality. In other words, does a treat a symptom of metabolic disorder, but not improve the underlying problem?

Statin RX may be overprescribed in healthy people without evidence of diseased arteries | e! Science News

2010-11-19T17:07:00.001-06:00

Statin RX may be overprescribed in healthy people without evidence of diseased arteries | e! Science News

A statistical comparison of results showed that few if any heart attacks or strokes would have been prevented within five years had anyone taken the medication, unless there was already some calcium buildup in their blood vessels. In people with moderate calcium buildup, one heart attack would have been averted in every 94 people treated, and one stroke in every 54.

For people with higher coronary calcium scores, the numbers of patients one needed to treat to prevent a heart attack or stroke were 24 and 19, respectively, which Blaha says were superior numbers to those in the JUPITER study or any prior statin trial.

According to study co-investigator and cardiologist Roger Blumenthal, M.D., a professor and director of the Ciccarone Preventive Cardiology Center at Johns Hopkins, "statin therapy should not be approached like diet and exercise as a broadly based solution for preventing coronary heart disease.

Statins are worth billions of dollars each year, and big pharma pushes doctors to push all of us to take them. Push back.

Low fat diets could increase heart disease risk, say nutrition experts

2010-11-16T19:06:00.001-06:00

Low fat diets could increase heart disease risk, say nutrition experts

Low fat diets could increase heart disease risk, say nutrition experts

By Caroline Scott-Thomas, 16-Nov-2010

Many Americans aim to eat low-fat foods but there is strong evidence that replacing fat with carbohydrates could be harmful to health, according to nutrition experts at the ADA conference in Boston last week.

Recommendations to reduce saturated fat intake are largely based on the notion that high levels increase risk of cardiovascular disease, but unless saturated fat is replaced with other fats, many studies have suggested that fat reduction could increase risk of heart disease.

During a symposium called “The Great Fat Debate: Is There Validity In the Age-Old Dietary Guidance?” at the American Dietetic Association’s (ADA) Food and Nutrition Conference and Expo, four leading experts presented evidence suggesting that low fat diets may be less healthy than those containing at least a moderate amount of fat. In particular, all four agreed that replacing saturated fat with carbohydrates – as has been widely recommended in the United States – is likely to raise the risk of cardiovascular disease.

The low fat message

Director of the cardiovascular health laboratory at Tufts University Dr. Alice Lichtenstein said dietary advice to adhere to a low fat diet is based on an oversimplification of recommendations.

[...]

“If anything, the literature shows a slight advantage of the high fat diet,” he said. “The focus on fat in dietary guidelines has been a massive distraction…We should remove total fat from nutrition facts panels on the back of packs.”

He added that while the pervasive dietary guidance given to consumers has been to eat fats sparingly, to load up on starch and eat non-fat products, “the food industry quickly realized sugar was cheaper than fat and laughed all the way to the bank.”

“It was really the type of fat that was important,” he said. “If you replaced saturated fat with polyunsaturated fat there was a reduction of risk.”

American eating behavior

[...]

Assistant professor of medicine at Harvard Medical School Dr. Mozaffarian agreed with the other speakers about a lack of evidence linking total fat consumption and cardiovascular disease risk.

High levels of low density lipoprotein (LDL cholesterol) and high triglyceride levels have both been linked to increased risk of cardiovascular disease, but Mozaffarian said there has often been overreliance on single biomarkers in drawing conclusions about fats’ impact on heart health, “even one as hallowed as LDL cholesterol”.

“Overall dietary quality is very important for cardiovascular risk,” he said. “Saturated fats may raise LDL cholesterol but increasing levels of all fats lowers triglycerides…You can’t look at data across countries and draw conclusions. Nor can you look at animal studies or a single biomarker and draw conclusions from that.”

Concluding the discussion, Dr. Lichtenstein warned against focusing on single nutrients for disease risk reduction.

She said: “We need to stop focusing on individual dietary components because when one goes down, another goes up.”

Wow, this is unbelievable. The American Dietetic Association is the bastion of Low Fat dogma. The fact that they are allowing dissenting voices is laudable and surprising. As positive evidence for low carb diets continues to mount, dietary advice is beginning to change as well. There is still much we don't know, but the biggest thing is to drop the dogma, do more research, and keep an open mind. Very good news here.

Renal Function Following Long-Term Weight Loss in Individuals with Abdominal Obesity on a Very-Low-Carbohydrate Diet vs High-Carbohydrate Diet

2010-11-15T14:21:00.001-06:00

Renal Function Following Long-Term Weight Loss in Individuals with Abdominal Obesity on a Very-Low-Carbohydrate Diet vs High-Carbohydrate Diet

Renal Function Following Long-Term Weight Loss in Individuals with Abdominal Obesity on a Very-Low-Carbohydrate Diet vs High-Carbohydrate Diet

Grant D. Brinkworth, PhDCorresponding Author Informationemail address, Jonathan D. Buckley, PhD, Manny Noakes, PhD, Peter M. Clifton, PhD

Accepted 4 September 2009.
Abstract

A frequently cited concern of very-low-carbohydrate diets is the potential for increased risk of renal disease associated with a higher protein intake. However, to date, no well-controlled randomized studies have evaluated the long-term effects of very-low-carbohydrate diets on renal function. To study this issue, renal function was assessed in 68 men and women with abdominal obesity (age 51.5±7.7 years, body mass index [calculated as kg/m2] 33.6±4.0) without preexisting renal dysfunction who were randomized to consume either an energy-restricted (∼1,433 to 1,672 kcal/day), planned isocaloric very-low-carbohydrate (4% total energy as carbohydrate [14 g], 35% protein [124 g], 61% fat [99 g]), or high-carbohydrate diet (46% total energy as carbohydrate [162 g], 24% protein [85 g], 30% fat [49 g]) for 1 year. Body weight, serum creatinine, estimated glomerular filtration rate and urinary albumin excretion were assessed before and after 1 year (April 2006-July 2007). Repeated measures analysis of variance was conducted. Weight loss was similar in both groups (very-low-carbohydrate: −14.5±9.7 kg, high-carbohydrate: −11.6±7.3 kg; P=0.16). By 1 year, there were no changes in either group in serum creatinine levels (very-low-carbohydrate: 72.4±15.1 to 71.3±13.8 μmol/L, high-carbohydrate: 78.0±16.0 to 77.2±13.2 μmol/L; P=0.93 time × diet effect) or estimated glomerular filtration rate (very-low-carbohydrate: 90.0±17.0 to 91.2±17.8 mL/min/1.73 m2, high-carbohydrate: 83.8±13.8 to 83.6±11.8 mL/min/1.73 m2; P=0.53 time×diet effect). All but one participant was classified as having normoalbuminuria at baseline, and for these participants, urinary albumin excretion values remained in the normoalbuminuria range at 1 year. One participant in high-carbohydrate had microalbuminuria (41.8 μg/min) at baseline, which decreased to a value of 3.1 μg/min (classified as normoalbuminuria) at 1 year.

This study provides preliminary evidence that long-term weight loss with a very-low-carbohydrate diet does not adversely affect renal function compared with a high-carbohydrate diet in obese individuals with normal renal function.

The myth that low carb hurts your kidneys refuses to die. Here's one more stake in the heart for it.

Intense Sweetness Surpasses Cocaine Reward

2010-11-13T16:05:00.002-06:00

PLoS ONE: Intense Sweetness Surpasses Cocaine Reward

Conclusions

Our findings clearly demonstrate that intense sweetness can surpass cocaine reward, even in drug-sensitized and -addicted individuals. We speculate that the addictive potential of intense sweetness results from an inborn hypersensitivity to sweet tastants. In most mammals, including rats and humans, sweet receptors evolved in ancestral environments poor in sugars and are thus not adapted to high concentrations of sweet tastants. The supranormal stimulation of these receptors by sugar-rich diets, such as those now widely available in modern societies, would generate a supranormal reward signal in the brain, with the potential to override self-control mechanisms and thus to lead to addiction.

I'm sure many people would nod their heads in agreement with the assertion that sweet treats are addictive. What was once a rare treat for our paleo ancestors is now everywhere, and hard to say no to. There's some evidence that upping magnesium intake may help people deal with sugar cravings. I have some magnesium articles on my blog here. Stick around and take a look!

Mid-Life Cholesterol Levels Not Linked to Alzheimer’s Disease

2010-11-13T16:04:00.001-06:00

Mid-Life Cholesterol Levels Not Linked to Alzheimer’s Disease

Mid-Life Cholesterol Levels Not Linked to Alzheimer’s Disease
Released: 11/2/2010 2:40 PM EDT
Embargo expired: 11/10/2010 4:00 PM EST
Source: American Academy of Neurology (AAN)

Newswise — Contrary to earlier research, a new, long-term study suggests that cholesterol level in mid-life may not be linked to later development of Alzheimer’s disease, according to a study published in the November 10, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology. However, the results suggest that large decreases in cholesterol levels in old age could be a better predictor of developing the memory-robbing disease.

“While some studies suggest that cholesterol is a risk factor for dementia, others have not replicated this finding, so the possible association has been under debate,” said study author Michelle M. Mielke, PhD, with Johns Hopkins University School of Medicine in Baltimore.

Paleo Ways Excerpt | Free The Animal

2010-11-13T12:56:00.002-06:00

Paleo Ways | Free The Animal:

"The Paleo Diet, Loren Cordain"

At first, humans were not terribly good hunters. They started out as scavengers who trailed behind predators such as lions and ate the leftovers remaining on abandoned carcasses. The pickings were slim; ravenous lions don't leave much behind, except for bones. But with their handy tools (stone anvils and hammers), our early ancestors could crack the skulls and bones and still find something to eat -- brains and fatty marrow.

Marrow fat was the main concentrated energy source that enabled the early human gut to shrink, while the scavenged brains contained a specific type of omega 3 fat called "docosahexaenoic acid" (DHA), which allowed the brain to expand. Docosahexaenoic acid is the building block of our brain tissue.

Without a dietary source of DHA, the huge expansion of our brain capacity could never have happened. Without meat, marrow, and brains, our human ancestors never would have been able to walk out of tropical Africa and colonize the colder areas of the world. If these people had depended on finding plant foods in cold Europe, they would have starved. In a landmark series of studies, my colleague Mike Richards, at Oxford University, studied the bones of Paleolithic people who lived in England some 12,000 years ago. Their diet, Richards confirmed, was almost identical to that of top-level carnivores, such as wolves and bears.

[...]

The archaeological record clearly shows that whenever and wherever ancient humans sowed seeds (and replaced the old animal-dominated diets), part of the harvest included health problems. One physical ramification of' the new diet was immediately obvious: Early farmers were markedly shorter than their ancestors. In Turkey and Greece, for example, preagricultural men stood 5 feet 9 inches tall and women 5 feet 5 inches. By 3000 the average man had shrunk to 5 feet 3 inches and the average woman to 5 feet. But getting shorter -- not in itself a health problem -- was the least of the changes in these early farmers. Studies of their bones and teeth have revealed that these people were basically a mess: They had more infectious diseases than their ancestors, more childhood mortality, and shorter life spans in general.

Teeth

They also had more osteoporosis, rickets, and other bone mineral disorders, thanks to the cereal-based diets. For the first time, humans were plagued with vitamin and mineral-deficiency diseases -- scurvy, beriberi, pellagra, vitamin A and zinc deficiencies, and iron-deficiency anemia. Instead of the well-formed, strong teeth their ancestors had, there were now cavities. Their jaws, which were formerly square and roomy, were suddenly too small for their teeth, which overlapped each other.

The First Butchers: 3.4 million old meat eaters!

2010-11-12T20:25:00.001-06:00

The First Butchers: Scientific American

A long time ago, by the shores of a lake in East Africa, a group of hungry foragers tucked into a primeval steak dinner. They carved the meat of cow- and goat-sized animals with sharp stone tools and smashed the bones to get at the rich marrow inside. The scene is remarkable mainly because it happened 3.4 million years ago, pushing back by 800,000 years the earliest known example of hominids using stone tools and eating meat.

The foragers in question were likely members of the primitive genus Australopithecus, specifically A. afarensis, the species to which the celebrated Lucy fossil belongs. Scientists had long believed that the australopithecines, whose teeth and jaws were adapted for eating fruit, seeds and other plant foods, were primarily vegetarian. But the new finds—cut-marked animal bones recovered from a site called Dikika, just a few kilometers from the Lucy site in Ethiopia’s Afar region—suggest that “we could now be looking at an extended period of time when [hominids] were including meat in their diet and experimenting with the use of stone tools,” observes lead study author Shannon P. McPherron of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. A report describing the bones appeared in the August 12 issue of Nature.

Children with hypertension more likely to have learning disabilities, ADHD

2010-11-10T12:53:00.001-06:00

Children with hypertension more likely to have learning disabilities, ADHD

Children with hypertension more likely to have learning disabilities, ADHD
10. November 2010 01:06

Children who have hypertension are much more likely to have learning disabilities than children with normal blood pressure, according to a new University of Rochester Medical Center (URMC) study published this week in the journal, Pediatrics. In fact, when variables such as socio-economic levels are evened out, children with hypertension were four times more likely to have cognitive problems.

"This study also found that children with hypertension are more likely to have ADHD (attention deficit hyperactivity disorder)," said Heather R. Adams, Ph.D., an assistant professor of Neurology and Pediatrics at URMC, and an author of the study. "Although retrospective, this work adds to the growing evidence of an association between hypertension and cognitive function. With 4 percent of children now estimated to have hypertension, the need to understand this potential connection is incredibly important."

Adult obesity linked to ADHD as child - UPI.com

2010-11-10T12:50:00.002-06:00

Adult obesity linked to ADHD as child - UPI.com

Researchers say there's a link between childhood ADHD and adult obesity, and the greater the number of ADHD symptoms a child has the more likely they may be to be overweight in adulthood. The study looked at symptoms of inattention, hyperactivity, and impulsivity along with body mass index for 15,197 teens who were studied between 1995 and 2009.

I saw a figure once that 70% of morbidly obese people have ADD. I really think there's a connection here. Scientists are beginning to learn that the brain itself can become insulin resistant. Perhaps that's why many people who do low carb or ketogenic diets to lose weight find themselves thinking more clearly, have more drive and a better mood.

Why do morphine-blocking drugs make you lose weight? The Heart Scan Blog:

2010-11-10T12:47:00.001-06:00

The Heart Scan Blog: Why do morphine-blocking drugs make you lose weight?

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Eating Patterns Vary Between Overweight Children And Normal Weight Children

2010-11-09T15:53:00.001-06:00

Eating Patterns Vary Between Overweight Children And Normal Weight Children

Overweight children reported more frequent intake of healthy foods such as fruit, vegetables, fish, brown bread and potatoes as well as low-energy cheese and yoghurt compared with normal weight children. This comes from a recent study from researchers at Telemark University College and the Norwegian Institute of Public Health.

The study showed that:

* Overweight children drank juice and artificially sweetened soft drinks more often, while the normal weight children drank carbonated drinks and ate unhealthy foods and processed foods such as burgers, sausages, biscuits, processed pizza and sweets.
* The results suggest that both parents and children have increased awareness of food choices when children are overweight.
* The study also showed that overweight children were less physically active and were more likely to have obese parents than normal weight children.

"It is positive that parents and children emphasise healthy food choices. However, it is important to note that the amount of healthy foods must be adapted to a child's activity level to limit further weight gain," said researcher Anne Lise Brantsæter at the NIPH.

Reference:
IM Oellingrath, MV Svendsen, AL Brantsæter. Eating patterns and overweight in 9- to 10-year-old children in Telemark County, Norway: a cross-sectional study. European Journal of Clinical Nutrition. 18. August 2010.

Lol, maybe the juice, fruit, bread, potatoes and low fat cheese made the kids fat. Cause you know if the study said the kids ate more meat it would be seen as "proof" meat causes obesity. Just sayin'

Hope for narcolepsy sufferers

2010-11-09T15:50:00.001-06:00

The science of sleep: hope for narcolepsy sufferers | Life and style | The Guardian

Around 25,000 people in the UK have narcolepsy, a condition characterised by sudden and uncontrollable episodes of deep sleep, often at times of stress or even sexual arousal. There's no known cure, but in terms of medical advances, 2010 has been lively.

As well as the reported alleged links to the swine flu vaccine in August – still unproven – Swiss researchers claimed in February to have identified the overproduction of an antibody, Trib2, in the immune systems of narcoleptics. Scientists at Geneva and Lausanne universities believe Trib2 is responsible for destroying hypocretin-secreting neurons in the brain. Hypocretin is a hormone that regulates sleep, so low levels interfere with non-REM (rapid-eye-movement) sleep and makes staying awake for long periods a struggle.

Excitingly, the tests suggested this damage could potentially be stabilised with intravenous immunoglobulin, a laboratory-made antibody. If patients could be diagnosed and treated within a year of symptoms presenting – when the antibodies are at their most destructive levels – the illness's impact could be greatly reduced. "There is a chance to save some of the hypocretin cells at early onset," says Professor Adrian Williams, who runs the sleep disorders centre at St Thomas's Hospital, London, and this year became the UK's first Chair in Sleep Medicine. "Unfortunately, narcolepsy is still under-recognised, and it is typically a few years between onset of symptoms – usually in the teens – and diagnosis."

Other studies indicate environmental factors that could "switch on" the gene for narcolepsy, which exists in a third of the population. In June, a Journal of Sleep Research paper reported a five-fold increase of the condition among genetically predisposed individuals who had suffered bacterial throat infections in childhood, while US studies suggested that exposure to heavy metals and gardening chemicals, as well as passive smoking, could be a trigger.

Perhaps the most significant development of recent years has been a medicine, Xyrem, whose active ingredient, sodium oxybate, is a derivative of the illicit substance GHB. Licensed here since 2006, it works by mimicking the activity of hypocretin.

DHA and EPA provided protection against insulin resistance and nonalcoholic fatty liver disease

2010-11-09T15:40:00.002-06:00

Media-Newswire.com - Press Release Distribution - PR Agency

Fish and other seafood are rich sources of the omega-3 fatty acids known as DHA and EPA, which have been found to provide protection from chronic diseases, such as type 2 diabetes, said LSU AgCenter nutritionist Beth Reames.

(Media-Newswire.com) - Fish and other seafood are rich sources of the omega-3 fatty acids known as DHA and EPA, which have been found to provide protection from chronic diseases, such as type 2 diabetes, said LSU AgCenter nutritionist Beth Reames.

In recent studies with animals, U.S. Department of Agriculture researchers have found that DHA provided protection against insulin resistance and nonalcoholic fatty liver disease, and EPA offered partial protection against fatty liver disease.

Insulin resistance is a condition in which the body isn’t able to efficiently use its own insulin to remove glucose from the bloodstream, Reames said. If left untreated, insulin resistance can lead to harmful buildup of glucose in the bloodstream and diabetes.

Nonalcoholic fatty liver disease results from accumulation of excess fat in the liver and may be caused by diabetes and obesity, Reames said. Afflicted liver tissue may harden and scar, sometimes resulting in cirrhosis of the liver or liver cancer.

“Human studies of the effects of DHA and EPA on insulin resistance have been inconclusive,” Reames said. “The researchers recommend new investigations, with larger numbers of volunteers, to more clearly define the relation of DHA and EPA to insulin resistance in humans.”

To get DHA and EPA in your diet, nutritionists recommend eating fatty or oily fish, including mackerel, sardines, anchovies, herring, albacore tuna and salmon, as well as oysters, shrimp, crawfish and fish oil supplements. In addition, omega-3 fatty acids are available from plant sources including soybean oil, canola oil, flaxseed and walnuts.

Omega-3 fatty acids help relax the arteries and improve blood circulation to the heart, inhibit blood clotting and improve heartbeat. They lower triglycerides and lower blood pressure. These factors make heart attacks less likely. They also keep the arteries open by discouraging the buildup of plaque in blood vessels.

Along with omega-3 fatty acids, fish and seafood offer additional health benefits. They are nutrient-dense and packed with protein.

Paleo humans ate MEAT! Stable Isotope Evidence for European Upper Paleolithic Human Diets

2010-11-06T01:27:00.001-05:00

SpringerLink - Abstract

Abstract
This paper presents the published and unpublished stable carbon and nitrogen isotope values for 36 European Upper Paleolithic humans from 20 sites. The isotope data were measured to determine the sources of dietary protein in Upper Paleolithic diets; the evidence indicates that animal, not plant, protein was the dominant protein source for all of the humans measured. Interestingly, the isotope evidence shows that aquatic (marine and freshwater) foods are important in the diets of a number of individuals throughout this period.

Humans have eaten a lot of meat throughout their history.

Increased adipose tissue lipolysis after a 2-week high-fat diet in sedentary overweight/obese men

2010-11-05T17:54:00.000-05:00

Increased adipose tissue lipolysis after a 2-week high-fat diet in sedentary overweight/obese men

Increased adipose tissue lipolysis after a 2-week high-fat diet in sedentary overweight/obese men

Harold R. Howe IIIa, Kimberly Heidalb, Myung Dong Choic, Ray M. Krausc, Kristen Boylec, Robert C. HicknercdeCorresponding Author Informationemail address

Received 21 January 2010; accepted 18 September 2010. published online 01 November 2010.
Corrected Proof
Abstract

The purpose of this study was to determine if a high-fat diet would result in a higher lipolytic rate in subcutaneous adipose tissue than a lower-fat diet in sedentary nonlean men. Six participants (healthy males; 18-40 years old; body mass index, 25-37 kg/m2) underwent 2 weeks on a high-fat or well-balanced diet of similar energy content (approximately 6695 kJ) in randomized order with a 10-day washout period between diets. Subcutaneous abdominal adipose tissue lipolysis was determined over the course of a day using microdialysis after both 2-week diet sessions. Average interstitial glycerol concentrations (index of lipolysis) as determined using microdialysis were higher after the high-fat diet (210.8 ± 27.9 μmol/L) than after a well-balanced diet (175.6 ± 23.3 μmol/L; P = .026). There was no difference in adipose tissue microvascular blood flow as determined using the microdialysis ethanol technique. These results demonstrate that healthy nonlean men who diet on the high-fat plan have a higher lipolytic rate in subcutaneous abdominal adipose tissue than when they diet on a well-balanced diet plan. This higher rate of lipolysis may result in a higher rate of fat mass loss on the high-fat diet; however, it remains to be determined if this higher lipolytic rate in men on the high-fat diet results in a more rapid net loss of triglyceride from the abdominal adipose depots, or if the higher lipolytic rate is counteracted by an increased rate of lipid storage.

Wow! Direct evidence of greater fat burning on a low carb, high fat diet.

Low-salt diet increases insulin resistance in healthy subjects

2010-11-05T03:18:00.001-05:00

Low-salt diet increases insulin resistance in healthy subjects

Low-salt diet increases insulin resistance in healthy subjects

Rajesh GargaCorresponding Author Informationemail address, Gordon H. Williamsa, Shelley Hurwitzab, Nancy J. Brownc, Paul N. Hopkinsd, Gail K. Adlera

Received 23 July 2010; accepted 11 September 2010. published online 01 November 2010.
Corrected Proof
Abstract

Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase insulin resistance (IR). We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals were studied after 7 days of LS diet (urine sodium <20 mmol/d) and 7 days of high-salt (HS) diet (urine sodium >150 mmol/d) in a random order. Insulin resistance was measured after each diet and compared statistically, unadjusted and adjusted for important covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range, 18-65) and with body mass index of 25.3 ± 4.0 kg/m2, were included in this study. Mean (SD) homeostasis model assessment index was significantly higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P < .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.

Not a big surprise, to me at least. Salt is an essential element, and our body regulates it carefully. The real cause of hypertension isn't salt, it's fructose, which causes increased uric acid. Check out this great presentation http://www.slideshare.net/nephron/uric-acid-fructose-and-hypertension

7 Myths and Information About Vegetarianism

2010-11-04T19:22:00.000-05:00

Myths and Information About Vegetarianism

Along with the saturated fat and cholesterol scares of the past several decades has come the notion that vegetarianism is a healthier dietary option for people. It seems as if every health expert and government health agency is urging people to eat fewer animal products and consume more vegetables, grains, fruits and legumes. Along with these exhortations have come assertions and studies supposedly proving that vegetarianism is healthier for people and that meat consumption causes sickness and death. Several medical authorities, however, have questioned these data, but their objections have been largely ignored.

As we shall see, many of the vegetarian claims cannot be substantiated and some are simply false and dangerous. There are benefits to vegetarian diets for certain health conditions, and some people function better on less fat and protein, but, as a practitioner who has dealt with several former vegans (total vegetarians), I know full well the dangerous effects of a diet devoid of healthful animal products.

It is my hope that all readers will more carefully evaluate their position on vegetarianism after reading this article. It is important to note that there are different types of vegetarianism, including lacto-vegetarian diets (dairy products included) and lacto-ovo-vegetarian diets (dairy products and eggs included). The nutritional caveats that follow are primarily directed at veganism, or a diet totally lacking in animal products.

Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet

2010-11-04T15:52:00.001-05:00

European Journal of Clinical Nutrition - Abstract of article: Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet

Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet

L A Frassetto1, M Schloetter1, M Mietus-Synder1, R C Morris Jr1 and A Sebastian1

1Department of Medicine, University of California San Francisco School of Medicine, San Francisco, CA, USA

Correspondence: Dr LA Frassetto, San Francisco School of Medicine, Campus box 0126 505 Parnassus Avenue, room 1202M San Francisco, CA 94143, USA. E-mail: frassett@gcrc.ucsf.edu

Received 25 July 2008; Revised 20 November 2008; Accepted 30 December 2008; Published online 11 February 2009.
Top of page
Abstract
Background:

The contemporary American diet figures centrally in the pathogenesis of numerous chronic diseases—‘diseases of civilization’. We investigated in humans whether a diet similar to that consumed by our preagricultural hunter-gatherer ancestors (that is, a paleolithic type diet) confers health benefits.
Methods:

We performed an outpatient, metabolically controlled study, in nine nonobese sedentary healthy volunteers, ensuring no weight loss by daily weight. We compared the findings when the participants consumed their usual diet with those when they consumed a paleolithic type diet. The participants consumed their usual diet for 3 days, three ramp-up diets of increasing potassium and fiber for 7 days, then a paleolithic type diet comprising lean meat, fruits, vegetables and nuts, and excluding nonpaleolithic type foods, such as cereal grains, dairy or legumes, for 10 days. Outcomes included arterial blood pressure (BP); 24-h urine sodium and potassium excretion; plasma glucose and insulin areas under the curve (AUC) during a 2 h oral glucose tolerance test (OGTT); insulin sensitivity; plasma lipid concentrations; and brachial artery reactivity in response to ischemia.
Results:

Compared with the baseline (usual) diet, we observed (a) significant reductions in BP associated with improved arterial distensibility (−3.1±2.9, P=0.01 and +0.19±0.23, P=0.05);(b) significant reduction in plasma insulin vs time AUC, during the OGTT (P=0.006); and (c) large significant reductions in total cholesterol, low-density lipoproteins (LDL) and triglycerides (−0.8±0.6 (P=0.007), −0.7±0.5 (P=0.003) and −0.3±0.3 (P=0.01) mmol/l respectively). In all these measured variables, either eight or all nine participants had identical directional responses when switched to paleolithic type diet, that is, near consistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.
Conclusions:

Even short-term consumption of a paleolithic type diet improves BP and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.
Keywords:

paleolithic diet, blood pressure, glucose tolerance, insulin sensitivity, lipids

In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee

2010-11-04T15:51:00.000-05:00

In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee

In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee

Adele H. Hite, M.A.T.a, Richard David Feinman, Ph.D.bCorresponding Author Informationemail address, Gabriel E. Guzman, Ph.D.c, Morton Satin, M.Sc.d, Pamela A. Schoenfeld, R.D.e, Richard J. Wood, Ph.D.f

Abstract

Concerns that were raised with the first dietary recommendations 30 y ago have yet to be adequately addressed. The initial Dietary Goals for Americans (1977) proposed increases in carbohydrate intake and decreases in fat, saturated fat, cholesterol, and salt consumption that are carried further in the 2010 Dietary Guidelines Advisory Committee (DGAC) Report. Important aspects of these recommendations remain unproven, yet a dietary shift in this direction has already taken place even as overweight/obesity and diabetes have increased. Although appealing to an evidence-based methodology, the DGAC Report demonstrates several critical weaknesses, including use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science. An objective assessment of evidence in the DGAC Report does not suggest a conclusive proscription against low-carbohydrate diets. The DGAC Report does not provide sufficient evidence to conclude that increases in whole grain and fiber and decreases in dietary saturated fat, salt, and animal protein will lead to positive health outcomes. Lack of supporting evidence limits the value of the proposed recommendations as guidance for consumers or as the basis for public health policy. It is time to reexamine how US dietary guidelines are created and ask whether the current process is still appropriate for our needs.

FANTASTIC take down of the latest dietary guidelines for americans, 2010 version. This is the report behind the food pyramid, mypyramid, and mypyramid.gov. Basically the whole food pyramid is based on sloppy science, and more importantly, misrepresenting the science that's out there. This report here just shreds the dietary guidelines put out by the federal government. Basically the evidence for fiber, fruits and vegetables, and low fat eating is just not there, despite decades of research designed to "prove" the lipid hypothesis. The feds keep trying to force a square peg into a round hole. Bottom line, avoid sugar, grains (especially processed), eat some fruits and veges, but don't get obsessive about it, and eat lots of quality meat. I would add preferably grassfed meat, and wild caught seafood. Real food, mostly meat, some plants, to paraphrase the author of the Omnivore's dilemma.

Low Carb Diet Better For Cardiovascular Health Than Low Fat Diet

2010-11-04T15:46:00.000-05:00

Low Carb Diet Better For Cardiovascular Health Than Low Fat Diet

Researchers from of the Center for Obesity Research and Education at Temple University, Philadelphia have revealed that after a two-year comparison, a low-carb diet fares about as well as a low-fat diet with regards to weight loss, but low-carb improves cardiovascular risk factors more.

The study, published in the peer-reviewed medical journal Annals of Internal Medicine, explained that cardiovascular risk factors, such as blood pressure and lipid (cholesterol) levels responded better with the low-carb diet. Both diets produce identical weight loss when coupled with comprehensive behavior treatment

Put simply - it appears that both diets are equally good for losing weight, but the low-carb diet protects you from potential coronary heart diseases more effectively.

[...]

Among the participants in the two diet groups, the researchers found:

* Weight - no differences at any point during the study. About 7% loss of weight at two years in both groups.
* Body composition - no differences at any point during the study
* Bone mineral density - no differences at any point during the study
* Good cholesterol levels - double the increase among the low-carb group compared to the low-fat group at two years. 23% and 11% respectively.

[...]

"Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet - A Randomized Trial"
Gary D. Foster, PhD, Holly R. Wyatt, MD, James O. Hill, PhD, Angela P. Makris, PhD, RD, Diane L. Rosenbaum, BA, Carrie Brill, BS, Richard I. Stein, PhD, B. Selma Mohammed, MD, PhD, Bernard Miller, MD, Daniel J. Rader, MD, Babette Zemel, PhD, Thomas A. Wadden, PhD, Thomas Tenhave, PhD, Craig W. Newcomb, MS, Samuel Klein, MD
Annals of Internal Medicine August 3, 2010 vol. 153 no. 3 147-157

More and more good research coming out on low carb the last few years, all of it good. When Atkins was big, people said "where's the evidence that this way of eating works and is safe?", but studies had not been done, because researchers were busy trying fruitlessly to "prove" fat was bad. Now that the attention is focused on low carb, the consensus of the research seems to indicate same or greater weight loss, on low carb vs. low fat, but much better readings on blood pressure, HDL, cholesterol, triglycerides, etc. This study is one of many.

Possible Link Between Personality And Exercise Levels

2010-11-04T15:42:00.000-05:00

Possible Link Between Personality And Exercise Levels

There may be a fundamental link between aspects of an individual's personality and their capacity to exercise or generate energy, recent research suggests.

Humans are not the only animals that choose to exercise and - as with people - individuals within the same species differ in their levels of activity, says Dr Peter Biro, a senior lecturer in the UNSW Evolution and Ecology Research Centre, in a review article in the journal Trends in Ecology and Evolution, with colleague Judy Stamps of the University of California, Davis. Dr Biro is an Australian Research Council Future Fellow.

Likewise, scientists now recognise that many animals have 'personality', in that they display consistent differences in behaviours. Dr Biro believes it is significant that those behaviours often relate to the rates at which they acquire and expend energy through feeding or activity.

"Some of us are couch potatoes while others are drawn to sport and exercise," notes Dr Biro. "We often associate the athletic 'jock' type or person with being aggressive and social, whereas the more sedentary 'nerd' often is seen as more socially awkward and submissive.

"These are generalisations, but most people would probably agree there is some truth to them. If so, why should individuals differ in their propensity for activity and in their personality, and why might they be related? "

The article reviews a wide range of recent research into these questions and concludes that there is now enough evidence to suggest a link between an individual's personality and the rate of its metabolism - the chemical process that converts food into the energy that fuels the body.

"Animals in captivity often engage in energetically demanding behaviour when they have unlimited food available," Dr Biro says. "Mice spend considerable time on running wheels, for example, and other animals often pace back and forth in zoo enclosures. Given they don't need to move about in search of food as they would in nature, we might ask why they are apparently 'exercising'.

"Recent research suggests that this behaviour might be related to an individual's capacity to generate energy - its 'metabolic capacity'. For example, mice in isolation that have high metabolism tend spend more time on running wheels, and run faster, than those with low metabolism.

"Male crickets with sex on their mind tend to call to attract mates more and have higher metabolism than those with slower metabolism."

Metabolism and aggression are also linked. It has now been documented, for example, in several species of fish and birds that individuals with high metabolism tend to be more aggressive and dominant over those with slow metabolism.

The amount of energy devoted to energetically demanding activities differs among individuals, Dr Biro says. These differences in energetic capacity - along with the tendency for metabolism to be consistent over long periods - might provide a very general explanation for personality in animals.

"It may just be that some individuals generate much more energy than others and when those individuals are captive with abundant food, they must outlet 'excess' energy that is normally expressed in nature in activities such as feeding and defence of food supplies.

"We are still some ways from a really solid understanding of the links between metabolism and personality in animals, but recent research suggests these ideas have merit and are worth studying further."

Source:
Bob Beale
University of New South Wales

When Dieting To Lose Weight, How Much You Sleep May Be As Important As How Much You Eat

2010-11-04T15:40:00.000-05:00

When Dieting To Lose Weight, How Much You Sleep May Be As Important As How Much You Eat

According to a new study being published in Annals of Internal Medicine, the flagship journal of the American College of Physicians, lack of sleep may hinder a dieter's ability to shed excess body fat.

Ten overweight but otherwise healthy adults on a moderate calorie-restricted diet were randomly assigned to sleep either 5.5 hours or 8.5 hours each night in a closed clinical research environment. After two weeks, researchers measured loss of fat and lean body mass. Compared to participants who slept 5.5 hours a night, the dieters that slept for 8.5 hours lost 56 percent more body fat. The dieters in the sleep restricted group had lost less fat and more lean body mass.

"These results highlight the importance of adequate sleep for maintenance of fat-free body mass when dieting to lose weight," said Plamen Penev, MD, PhD, Assistant Professor, Section of Endocrinology, at the University of Chicago and lead author of the study.

While measuring fat loss was the primary objective of the study, researchers also assessed other factors including levels of hormones that affect the appetite and weight. In addition, participants in both groups were asked to report how much hunger they experienced during the study.

"Among other hormonal effects, we found that sleep restriction caused an increase in ghrelin levels in the blood," said Dr. Penev. "Ghrelin is a hormone that has been shown to reduce energy expenditure, stimulate hunger and food intake, promote retention of fat, and increase glucose production in the body. This could explain why sleep-deprived participants also reported feeling hungrier during the study."

Why Fish Oils Can Improve Diabetes Control

2010-11-04T15:39:00.000-05:00

Why Fish Oils Can Improve Diabetes Control

Olefsky and colleagues looked at cellular receptors known to respond to fatty acids. They eventually narrowed their focus to a G-protein receptor called GPR120, one of a family of signaling molecules involved in numerous cellular functions. The GPR120 receptor is found only on pro-inflammatory macrophages in mature fat cells. When the receptor is turned off, the macrophage produces inflammatory effects. But exposed to omega-3 fatty acids, specifically docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), the GPR120 receptor is activated and generates a strong anti-inflammatory effect.

Olefsky, a professor of medicine and associate dean of scientific affairs for the UC San Diego School of Medicine stated that, "It's just an incredibly potent effect… The omega-3 fatty acids switch on the receptor, killing the inflammatory response."

The scientists conducted their research using cell cultures and mice, some of the latter genetically modified to lack the GPR120 receptor. All of the mice were fed a high-fat diet with or without omega-3 fatty acid supplementation. The supplementation treatment inhibited inflammation and enhanced insulin sensitivity in ordinary obese mice, but had no effect in GPR120 knockout mice. A chemical agonist of omega-3 fatty acids produced similar results.

"This is nature at work," said Olefsky. "The receptor evolved to respond to a natural product -- omega-3 fatty acids -- so that the inflammatory process can be controlled. Our work shows how fish oils safely do this, and suggests a possible way to treating the serious problems of inflammation in obesity and in conditions like diabetes, cancer and cardiovascular disease through simple dietary supplementation."

However, Olefsky said more research is required. For example, it remains unclear how much fish oil constitutes a safe, effective dose. High consumption of fish oil has been linked to increased risk of bleeding and stroke in some people.

Fasting Alters Pulsatile and Rhythmic Cortisol Release in Normal Man -- VANCE and THORNER 68 (6): 1013 -- Journal of Clinical Endocrinology & Metabolism

2010-11-04T15:38:00.000-05:00

Fasting Alters Pulsatile and Rhythmic Cortisol Release in Normal Man -- VANCE and THORNER 68 (6): 1013 -- Journal of Clinical Endocrinology & Metabolism

Fasting Alters Pulsatile and Rhythmic Cortisol Release in Normal Man*
MARY LEE VANCE and MICHAEL O. THORNER

Department of Internal Medicine, University of Virginia Medical Center Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Mary Lee Vance, M.D., Box 511, University of Virginia Medical Center, Charlottesville, Virginia 22908.

The effect of a 5-day fast on integrated, pulsatile, and periodic cortisol release was studied in 10 normal men by measuring serum cortisol concentrations every 20 min for 24 h before (day 0) and during the fifth day of fasting (day 5). Serum concentration profiles were analyzed for integrated cortisol release (area under the curve), pulsatile hormone release by an objective, statistically based pulse detection algorithm (cluster analysis), and periodic hormone release (circadian and ultradian rhythms) by Fourier expansion time series analysis. Urinary cortisol excretion per 24 h was measured in 5 men. The mean 24-h integrated serum cortisol concentration increased 1.7-fold during fasting (P = 0.0006). This increase resulted from a 2-fold increase in the serum cortisol concentrations between pulses (valley mean; P = 0.0004), an increase in the pulse height (P = 0.001), and an increase in pulse increment above baseline (P = 0.01). There were no changes in the number of pulses per 24 h, the interval between pulses, the width of the pulses, or the area of the pulses during fasting. Twenty-four-hour urinary cortisol excretion increased in all men, and the mean urinary cortisol (nanomoles per L)/creatinine clearance (milliliters per s) ratio increased from 119 on day 0 to 187 on day 5 (n = 5; P = 0.05). The pattern of periodic hormone release also changed during fasting; the mean (±SE) circadian rhythm (24-h) amplitude decreased from 160 ± 14 nmol/L on day 0 to 102 ± 105 nmol/L on day 5 (P = 0.06), and the amplitude of the 12-h rhythm increased from 68 ± 11 to 99 ± 11 nmol/L. There also were significant increases in the amplitudes of rhythms with periodicities of 8.1, 4.1, 2.4, 1.6, and 1.3 h (P = 0.02–0.008). Fasting in normal men results in distinct changes in the amount and pattern of pulsatile, circadian, and ultradian cortisol release.

Another study on fasting and cortisol, the stress hormone. Fasting makes you less stressed, eating glucose (bread, sugar), makes you more stressed, or stressable.

Effects of Fasting and Glucose Load on Free Cortisol Responses to Stress and Nicotine -- Kirschbaum et al. 82 (4): 1101 -- Journal of Clinical Endocrinology & Metabolism

2010-11-04T15:37:00.000-05:00

Effects of Fasting and Glucose Load on Free Cortisol Responses to Stress and Nicotine -- Kirschbaum et al. 82 (4): 1101 -- Journal of Clinical Endocrinology & Metabolism

Effects of Fasting and Glucose Load on Free Cortisol Responses to Stress and Nicotine1
Clemens Kirschbaum, Esperanza Gonzalez Bono, Nicolas Rohleder, Claudius Gessner, Karl Martin Pirke, Alicia Salvador and Dirk Helmut Hellhammer

Center for Psychobiological and Psychosomatic Research University of Trier (C.K., N.R., C.G., K.M.P., D.H.H.), Trier, Germany; and Area of Psychobiology, Department of Psychology, University of Valencia (E.G.B., A.S.), Valencia, Spain

Address all correspondence and requests for reprints to: Clemens Kirschbaum, Center for Psychobiological and Psychosomatic Research, University of Trier, Universitaetsring 15, D-54286 Trier, Germany. E-mail: kirschba@uni-trier.de.

The availability of energy appears to exert important regulatory functions in pituitary-adrenal stress responses. In two studies, the effects of short-term fasting and subsequent glucose administration on the free cortisol response to psychological stress and nicotine consumption were investigated. Study 1: After fasting for 8–11 h, healthy young men ingested either 100 g glucose (n = 13) or water (n = 12). One hour later they were exposed to a psychosocial stress task (Trier Social Stress Test). A third group also ingested 100 g glucose, but they were not exposed to any additional treatment (n = 10). Capillary blood glucose levels were in the lower euglycemic range before and significantly elevated after the glucose load (64.9 ± 9.8 vs. 162.5 ± 43.5 mg/dL; F = 149.04, P < 0.001). Although glucose load per se did not affect free cortisol levels, psychosocial stress induced a large cortisol response in glucose-treated subjects. In contrast, fasted subjects who received tap water did not respond to the Trier Social Stress Test with significant changes in cortisol levels (F = 6.27, P < 0.001). Both groups responded with a similar increase in heart rates (F = 33.53, P < 0.001) with no statistically significant difference between glucose and water-treated subjects. Study 2: Twelve habitual smokers received 100 g glucose or tap water after fasting for at least 8 h on two separate sessions (cross-over, random sequence). Forty-five min after glucose/water ingestion, they smoked two cigarettes with a nicotine content of 1.0 mg/cigarette. Subjects were euglycemic before smoking, with a significant rise of glucose levels after consumption of 100 g glucose (64.4 ± 8.3 vs. 143.5 ± 40.0 mg/dL; F = 40.25, P < 0.001). As in Exp 1, subjects showed a substantially larger free cortisol response to nicotine under glucose load compared with water load (F = 4.91, P < 0.001).

From these data we conclude that the free cortisol response to stimulation is under significant control of centers responsible for monitoring energy availability. Low glucose levels appear to inhibit adrenocortical responsiveness in healthy subjects. In agreement with results from animal studies, the present results suggest that ready access to energy is a prerequisite for hypothalamus-pituitary-adrenal stress responses.

So consuming glucose makes your stress level go up faster. Look at all of us, eating carbs 3-5 times a day, and how stressed out we are. Recipe for road rage and stress overload.

Why Fish Oils Can Improve Diabetes Control

2010-10-22T16:47:00.000-05:00

Why Fish Oils Can Improve Diabetes Control

Researchers at the University of California, San Diego School of Medicine have identified the molecular mechanism that makes omega-3 fatty acids so effective in reducing chronic inflammation and insulin resistance…
Advertisement

The discovery could lead to development of a simple dietary remedy for many of the more than 23 million Americans suffering from diabetes and other conditions.

Writing in advance of publication, Jerrold Olefsky, MD, and colleagues identified a key receptor on macrophages abundantly found in obese body fat. Obesity and diabetes are closely correlated. The scientists say omega-3 fatty acids activate this macrophage receptor, resulting in broad anti-inflammatory effects and improved systemic insulin sensitivity.

Macrophages are specialized white blood cells that engulf and digest cellular debris and pathogens. Part of this immune system response involves the macrophages secreting cytokines and other proteins that cause inflammation, a method for destroying cells and objects perceived to be harmful. Obese fat tissue contains lots of these macrophages producing lots of cytokines. The result can be chronic inflammation and rising insulin resistance in neighboring cells over-exposed to cytokines. Insulin resistance is the physical condition in which the natural hormone insulin becomes less effective at regulating blood sugar levels in the body, leading to myriad and often severe health problems, most notably Type 2 diabetes.

Consequences of Malnutrition, Fasting, Stress and Disease - Nutrition Partner B. Braun

2010-10-22T01:56:00.000-05:00

Consequences of Malnutrition, Fasting, Stress and Disease - Nutrition Partner B. Braun

4. Consequences of fasting, stress and disease

Fasting and stress have opposite influences on the energy expenditure of the human organism. The healthy human body is capable of passing from a state involving three regular food intakes to a state of short-term fasting and even prolonged fasting, as a result of precise metabolic regulation. In these cases, the organism will save as much energy as possible, thus reducing energy expenditure.

However, in stress conditions, energy expenditure is markedly increased. As a result, the body´s metabolism will be converted into a catabolic state, the gravity of which is determined by the nature and degree of the injury and type and severity of underlying disease.

These and other processes will be developed in the following chapters.

[Table of contents]

4.1 Effects of fasting

In theory, if a person having 15 kg of adipose triglycerides — i.e. 140.000 kcal of reserves in the form of fats (Cahill, 1970)— and energy requirements of 1800 kcal/day, begins to fast, he should be capable of withstanding 75 days of total fasting. In practice, an abstinence from feeding leads to death after about 50 days of total fasting. In other words, the theoretical value of the energy reserves can not be used in its entirety, because death intervenes beforehand due to partial depletion of functional tissue proteins.

In the case of abstinence or fasting, endogenous energy stores are used for metabolic processes. Fat, stored in indifferent fat tissue, is the major source of energy. Energy can also be derived from protein; however, there is no indifferent protein tissue and as a consequence the loss of protein always leads to a loss of organ function.

Hence, in the case of fasting in healthy persons, the metabolism is aimed at keeping the loss of protein as low as possible by lowering the metabolism and the gluconeogenesis. The loss of nitrogen is reduced in the case of complete fasting from 10 g per day to 4 - 5 g a day after 3 weeks. Fat stores are depleted faster with the purpose of providing energy.

Many organs including the heart, kidneys and muscles, can use either fatty acids or ketone bodies, derived from partial oxidation of fatty acids, directly as energy substrates. The central nervous system, on the other hand, and the red blood cells can only use glucose as an energy substrate. For example, during a 24 hour fast, the brain will consume 150 g of glucose and the other organs about 36 g, i.e. a total of 186 g of glucose per day. Since the body is incapable of synthesizing glucose from fat, it uses other substrates for gluconeogenesis. In fact, the glycogen reserves are insufficient to cover the requirements for more than 1 day. The most important substrate for gluconeogenesis is provided by amino acids and, to a minor extent, by glycerol derived from the triglycerides.
Metabolism of short-term fasting
Fig. 8: Metabolism of short-term fasting

In short-term fasting, some of the glucose required by the brain is provided by liver glycogen, the reserve being exhausted within 48 hours. If the human body is to withstand fasting, it must mobilize 1800 kcal/day and produce 186 g of glucose mainly for the central nervous system. Eighty percent of the energy requirements are provided by lipolysis of adipose tissue where 160 g of triglycerides are split into fatty acids and glycerol. Approximately 75 g of muscle proteins, i.e. nearly 300 g of muscle, per day are mobilized to provide the substrate for gluconeogenesis. If protein breakdown were to continue at the initial rate, roughly one-third of the total body proteins would be exhausted in 3 weeks, which is incompatible with survival.

So, if fasting is prolonged, a major metabolic adaptation occurs. The central nervous system begins to use ketone bodies as an energy substrate, thereby reducing glucose requirements. Therefore, in prolonged fasting, there is a shift from the use of protein as an energy source towards the use of fats (in the form of ketone bodies). This adaptation permits protein sparing and preserves the proteins' functional role. Nevertheless, obligatory proteolysis always persists, amounting in the foregoing example to at least 20 g of protein daily.
Metabolism of short-term fasting
Fig. 9: Metabolism of prolonged fasting

Metabolic processes respond to internal signals. During fasting, blood glucose levels fall with a consequent reduction in the secretion of insulin and an increase in glucagon, two hormones with antagonistic actions on energy metabolism. As a result of the decrease in the circulating insulin level, triglyceride catabolism increases, causing the release of free fatty acids and glycerol. The raised glucagon levels lead initially to a distinct increase in liver glycogenolysis. Further, gluconeogenesis is stimulated by glucagon, which inhibits protein synthesis and stimulates muscular proteolysis, thereby furnishing the amino acid substrate.

There is therefore a metabolic adaptation to prolonged fasting, resulting in a reduction of energy expenditure of up to 40% (Goldstein and Elwyn, 1989; Kinney, 1970). These mechanisms, which tend to limit proteolysis in the healthy person, are defective or non-operative in cases of severe disease or stress, as will be discussed in the next chapter.

Vegetarian Indians more likely to suffer heart disease--study | TheMedGuru

2010-10-21T15:01:00.000-05:00

Vegetarian Indians more likely to suffer heart disease--study | TheMedGuru:

"On the occasion of World Heart Day (September 26) there’s a bad news for vegetarians Indians. As per a new research report presented by a Pune-based bariatric Dr. Shashank Shah, vegetarian Indians are more prone to suffer from heart ailments.

Commenting on why veggie Indians are more at risk of heart diseases, Dr. Shah said in a press statement, “We found that Indians are grossly deficient in vitamin B12, which is a crucial cardio-protective factor in the body.

Vitamin B12 is usually found in food that comes from animals, like fish, meat, poultry, milk and milk products. However, since a lot of Indians are vegetarians, they do not get adequate amounts of vitamin B12 in their diet.”"

[...]

Details of research study
To come to this startling conclusion Dr Shah along with his colleague Dr Todkar, studied the data collected from about 300 patients from Hiranandani Hospital, Powai, over the period of one year.

They were startled to find out that 70 percent of these patients had suffered from a cardiac [pertaining to the heart.] disease or are at greater risk of cardiac attack in near future.

Nearly all of them were found to be suffering from vitamin B12 deficiency.

“When vitamin B12 levels fall, homocysteine levels increase. The latter is known to cause atherosclerosis (hardening and narrowing of the arteries), as well as an increased risk of heart attacks, strokes and blood clot formation,” noted Dr Shah in his study report.

Science trumps politics: urinary sodium data challenge US dietary sodium guideline -- McCarron et al. 92 (5): 1005 -- American Journal of Clinical Nutrition

2010-10-20T18:40:00.000-05:00

Science trumps politics: urinary sodium data challenge US dietary sodium guideline -- McCarron et al. 92 (5): 1005 -- American Journal of Clinical Nutrition

Science trumps politics: urinary sodium data challenge US dietary sodium guideline1,2
David A McCarron, Tilman B Drüeke and Edward M Stricker

1 From the Department of Nutrition, University of California, Davis, CA (DAM); INSERM ERI-12, UFR de Médecine et de Pharmacie, Université de Picardie Jules Verne, Amiens, France (TBD); and the Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA (EMS).

2 Address correspondence and reprint requests to DA McCarron, The McCarron Group, 120 NW Ninth Avenue, Portland, OR 97209. E-mail: dmccarron@mccarrongroup.com.

See corresponding article on page 1172.

For the past 3 decades, the US government has promoted a policy of reduced dietary sodium intake as the principal nutritional means of reducing blood pressure and its attendant cardiovascular disorders in adults. Early on, this policy targeted at-risk individuals such as people with chronic arterial hypertension; however, in the past decade it has been applied to the population at large. Despite a litany of well-intended strategies from mandatory sodium labeling to extensive educational and social marketing efforts, there is little evidence that sodium intake has changed. In fact, some advocates of the policy have argued that sodium intake actually has increased, reaching extreme levels in some people (1). The failure of the government's efforts has been typically attributed to the food industry's excessive use of sodium in their products (1). Both the application of such a government policy to the entire population and the simplistic assessment that its failure to date can be attributed to the food industry's reluctance to provide lower sodium foods belie the scientific complexity of the issues, including sodium's role in health and disease.

In this issue of the Journal, Bernstein and Willett (2) provide a valuable analysis of 24-h urinary sodium (UNaV) data extracted from the medical literature published between 1957 and 2003. Their findings from the 38 US studies that met rigorous search criteria and involved 26,271 people confirm and extend the conclusions we published a year ago (3). Our analysis involved 19,151 people from 33 countries and 62 survey sites between 1984 and 2008. Like that of Bernstein and Willett, our analysis revealed a remarkably narrow range of UNaV across very diverse populations and eating habits, without the extreme levels often purported to exist by advocates of lower sodium intake (1) and no evidence of a change over time. The latter was best shown by the data of the UK Food Standards Agency between 1986 and 2008, which we noted (3) offered no evidence that an intense social marketing effort begun in 2005 had been successful.

One possible explanation, first raised by our report last year (3), is that human sodium intake is a parameter that even the most well intentioned public policy cannot modify in most people. An extensive body of basic science research, dating from Richter's seminal observations (4), has characterized an integrated network of peripheral hormonal signals interfaced with complex neural networks specific to regulating sodium intake of experimental animals (5). Although those basic research findings have not as yet been extrapolated to humans, they should not be completely ignored because they may yet provide a model of what is feasible in humans.

The current report extends our observations by documenting that, likewise, all the efforts in the United States over the past 3 decades have had no effect on the population's sodium intake. An alternative possibility for the stability of sodium intake is that sodium has been largely consumed in association with food intake, motivated by hunger and appetite. To the extent that caloric intake has been stable over populations and decades, so too has sodium. Thus, a potential benefit of reducing food sodium content would be a concurrent reduction of sodium. Working against that theoretical outcome, however, is the reality that over the millennia, before the introduction of processed foods, sodium was added to foods at the time of preservation, cooking, or consumption. An individual in our society has the identical options today as the food industry moves to offering more products whose ratio of calories to sodium is increased (ie, lower sodium content per serving). This individual choice could abrogate any effect on average sodium intake in society as these data indicate has happened.

Regardless of why sodium intake has been so stable, the data of Bernstein and Willett (2), as well those of McCarron et al (3), suggest that it is not a readily modifiable nutritional parameter for the population at large. Furthermore, a substantial body of research in humans provides evidence as to why this latest attempt to modify the general population's sodium intake is doomed to failure. Sodium has a critical role in extracellular fluid volume regulation as well as being of fundamental importance in cellular function across virtually all organ systems. Thus, it is unlikely that as an organism, humans would have evolved without the development of failsafe mechanisms to ensure sufficient sodium availability. Sodium is 1 of only 3 nutrients whose excretion in urine is recognized as regulated; water and glucose are the other 2. Consequently, deficits in these nutrients elicit immediate, potent, counterregulatory physiologic responses.

Changes in lipoprotein(a), oxidized phospholipids, and LDL subclasses with a low-fat high-carbohydrate diet — The Journal of Lipid Research

2010-10-17T00:40:00.000-05:00

Changes in lipoprotein(a), oxidized phospholipids, and LDL subclasses with a low-fat high-carbohydrate diet — The Journal of Lipid Research

Changes in lipoprotein(a), oxidized phospholipids, and LDL subclasses with a low-fat high-carbohydrate diet

1. Nastaran Faghihnia*,
2. Sotirios Tsimikas†,
3. Elizabeth R. Miller†,
4. Joseph L. Witztum† and
5. Ronald M. Krauss*,1

+ Author Affiliations

1.
*Department of Atherosclerosis Research, Children's Hospital Oakland Research Institute, Oakland, CA
2.
†Department of Medicine,† University of California, San Diego, La Jolla, CA

Abstract

Low-fat diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)], a preferential lipoprotein carrier of oxidized phospholipids (OxPLs) in plasma, as well as small dense LDL particles. We sought to determine whether increases in plasma Lp(a) induced by a low-fat high-carbohydrate (LFHC) diet are related to changes in OxPL and LDL subclasses. We studied 63 healthy subjects after 4 weeks of consuming, in random order, a high-fat low-carbohydrate (HFLC) diet and a LFHC diet. Plasma concentrations of Lp(a) (P < 0.01), OxPL/apolipoprotein (apo)B (P < 0.005), and OxPL-apo(a) (P < 0.05) were significantly higher on the LFHC diet compared with the HFLC diet whereas LDL peak particle size was significantly smaller (P < 0.0001). Diet-induced changes in Lp(a) were strongly correlated with changes in OxPL/apoB (P < 0.0001). The increases in plasma Lp(a) levels after the LFHC diet were also correlated with decreases in medium LDL particles (P < 0.01) and increases in very small LDL particles (P < 0.05). These results demonstrate that induction of increased levels of Lp(a) by an LFHC diet is associated with increases in OxPLs and with changes in LDL subclass distribution that may reflect altered metabolism of Lp(a) particles.

Comment- Pretty straight up study, and low carb wins big time. Lipoprotein a, apo B, and oxidizzed phospolipids are all important markers of heart disease, and all of them got worse on low fat, better on low carb.

Confirmatory Evidence of Cancer-Nutrition Link Remains Elusi... : Oncology Times

2010-10-16T19:20:00.000-05:00

Confirmatory Evidence of Cancer-Nutrition Link Remains Elusi... : Oncology Times

Confirmatory Evidence of Cancer-Nutrition Link Remains Elusive
Goodman, Alice
Free Access

SAN FRANCISCO-Although a link between nutrition and cancer was posited as long ago as ancient China, modern studies have been only partly successful in illuminating this association, explained Arthur Schatzkin, MD, DrPH, of the NCI's Nutritional Epidemiology Branch, speaking here at the American Society of Clinical Oncology Annual Meeting at a Scientific Symposium on Nutrition and Cancer.

Do we have hard, credible evidence that nutritional modification can truly affect the incidence of malignant disease in humans? The answer, in short, is a resounding maybe. We are getting there, but nutrition and cancer is a complex and difficult field. When it comes to nutrition, the evidence is softer and vulnerable to the results of the latest analysis or published paper.

The dearth of hard evidence coupled with inherent difficulties in conducting valid studies in this area has led to confusion and inconsistency about the role of nutrition in the risk of developing cancer.

Obstacles to conducting studies of nutritional epidemiology of cancer cited by Dr. Schatzkin include: exposure assessment error (is the right dietary factor being studied and are the right questions being asked?), inadequate range of exposure (many populations have narrow intake distributions for certain potentially cancer-related nutrients and foods), and confounding (people who follow a certain type of diet may also differ in biologic or lifestyle factors that are related to the risk of developing cancer).

Randomized, controlled trials largely circumvent the problem of confounding, and results from such studies are extremely compelling, Dr. Schatzkin continued. However, these studies are expensive and logistically complex to mount.

At present, Dr. Schatzkin said it is difficult to make recommendations with certainty regarding controversial areas such as the relationship of dietary fat intake and breast cancer; the role of dietary fiber and colorectal cancer; and the role of vitamins/supplements (i.e., beta carotene and lung cancer, lycopene, and prostate cancer, and folic acid and colorectal cancer). The hope is that future studies will help to resolve these issues.

Cancer Prevention Diet, RIP

2010-10-16T19:14:00.000-05:00

Cancer Prevention Diet

In Fact, Only a Guess

But even this was only a guess. "We have attributed the largest risk to dietary factors," they wrote. "It must be emphasized the figure chosen is highly speculative and chiefly refers to dietary factors which are not yet reliably identified."

However, even by 1981 two possible preventive factors, beta-carotene and other precursors of Vitamin A, and dietary fiber were already identified. It was a satisfying overall package. Beta-carotene was an antioxidant, and there was some evidence that antioxidants might have a role in preventing the No. 1 cancer killer, lung cancer. Fiber seemed to have a preventive role in the No. 2 cancer--colorectal cancer-and eating more fiber usually meant a lower fat diet, and both animal and vegetable fats were also suspects in increasing cancer risk.

Finally, these theories nicely fit the dietary recommendations that had already been made. While the scientific literature grew to include literally hundreds of studies examining these issue from some narrow perspective, the scientists at the National Cancer Institute understood that convincing scientific evidence was going to be achieved with only one scientific technique: the randomized clinical trial.

In a clinical trial intervention study, the only meaningful difference between a treatment group and an untreated control group is the chemical or food item under study. The best studies are double blind, with neither investigator nor volunteer knowing whether they are receiving the active treatment, or a placebo.
Beta-carotene on Trial

Beta-carotene was the first to be studied in such trials, but researchers used a dietary supplement pill rather than foods. The pill had a known quantity of the chemical under study, could be given in a double blind trial using a placebo, and did not involve the experimental complexities of trying to modify diet in a consistent fashion for years on end.

Enthusiasts believed that beta-carotene had wondrous powers-that it might be an antioxidant, boost the immune system, and even inhibit the formation of cancerous cells. This evidence came from bench biochemistry, experiments with cells in petri dishes, and examinations of large populations of people where many, many factors could be involved. Now this idea was being tested in a manner that might provide definitive scientific evidence of the benefit to ordinary people.

As a National Academy of Sciences panel recently noted, not one major trial of beta-carotene produced any evidence of a beneficial effect on cancer, and one study suggested a possible harmful effect. Whether beta-carotene was studied in low risk patients (22,000 practicing physicians), or among high risk asbestos workers and heavy smokers, no benefit was seen in studies of 8 to 12 years duration.
Fiber and Fruit to the Test

Fiber, fruits, vegetables-the heart of the "5 a day program" --were the next to be systematically studied in clinical trials. One central problem in studying cancer is that despite it being the second ranked cause of death, cancer is quite rare in any group of healthy people and therefore requires studying literally tens of thousands for many years to acquire a few dozen cases of the specific cancer of interest.

However, colon cancer begins as benign polyps and adenomas that only later become malignant. By leaving out all the thousands of people who were not at great risk anyway, and focusing on people who already developed the earliest precursors, the investigators could learn much more about fiber in trials of only a few thousand patients.

Still the problem of modifying diet remained. In one study participants were given one of two identical-looking breakfast cereals from Kellogg that contained either 13 grams of additional fiber or just 2 grams. The second study attempted and achieved a broader dietary modification. Through training and counseling sessions, the intervention group was induced to increase fiber by 75 percent, boost their number of servings of fruits and vegetables by two thirds; and to reduce the fat in their diet. The other group was not counseled and food intake remained largely unchanged.

In both studies the intervention was foods rather than the purified chemical ingredient. In both studies real dietary changes were maintained for three to four years. Nevertheless, no effect whatever was found on the recurrence of polyps or adenomas in either study. Fiber, fruits and vegetables worked no better in preventing cancer than had beta-carotene

Evidence Summary: Dietary fiber supplements and obesity

2010-10-16T19:09:00.000-05:00

Evidence Summary: Dietary fiber supplements and obesity

Dietary fiber supplements and obesity

Evidence Summary

Fiber supplements were defined, for the purposes of this project, as fibers which have been isolated from the original source. The fiber may be incorporated into foods and beverages or taken as a pill or powder.

Body Weight

11 studies: Three positive-rated randomized controlled trials (Birketvedt et al, 2005; Rossner et al, 1987; Ryttig et al, 1989), five neutral-rated randomized controlled trials (Birketvedt et al, 2000; Hylander et al, 1983; Pasman, Westerterp-Plantenga et al, 1997; Rigaud et al, 1990; Solum et al, 1987) and three positive-rated randomized controlled trials with crossover (Kovacs et al, 2001; Meada et al, 2005; Vuksan et al, 1999), examined the impact of fiber supplements on body weight in overweight and obese individuals.

Increased Weight Loss

Seven studies found increased weight loss with fiber supplement intake of 0.8g to 20g for five weeks to 14 months (Birketvedt, 2000; Birketvedt, 2005; Pasman and Westerterp-Plantenga, 1997; Rigaud, 1990; Rossner, 1987; Ryttig, 1989; Solum, 1987).

* Increased weight loss
o Birketvedt, 2000, 24 weeks: 1,200-kcal diet (15g per day dietary fiber) plus fiber supplement (grain and citrus fiber; 85% insoluble) or control; Weeks One to Eight, six grams per day; Weeks Nine to 24, four grams per day
o Birketvedt, 2005, five weeks: 1,200-kcal diet plus fiber supplement or control; Glucosahl, 6.1g (4.32g glucomannan, 0.9g guar, 0.9g alginat); Chrombalance, 1.24g (1.24g glucomannan) or Appe-Trim, 0.84g (0.42g glucomannan, 0.42g guar)
o Pasman and Westerterp-Plantenga, 1997, 14 months: 16g to 20g guar gum, 10g to 15g guar gum or control
o Rigaud, 1990, six months: Seven grams per day insoluble fiber supplement (beet, barley, citrus; 90% insoluble) or placebo
o Rossner, 1987, three months: 1,400-kcal diet with five grams per day fiber supplement (grain and citrus fiber) or placebo; two months AND 1,600-kcal diet with seven grams per day fiber supplement (vegetable, grain and citrus fiber) or placebo
o Ryttig, 1989: 1,200-kcal diet with seven grams per day fiber supplement or placebo for 11 weeks, then 1,600-kcal diet with six grams per day fiber supplement or placebo for 16 weeks, then ad lib diet with six grams per day fiber supplement for 25 weeks
o Solum, 1987, 12 weeks: 1,200-kcal diet (25g per day dietary fiber) with six grams per day fiber supplement (grain and citrus fiber) or control.

No Increase in Weight Loss

Four studies found no increase in weight loss with 4.5g to 6.6g fiber supplementation for two to 12 weeks (Hylander, 1983; Kovacs, 2001; Meada, 2005; Vuksan, 1999).

* No difference in weight loss
o Hylander, 1983, three weeks: 6.6g ispaghula, 6.6g bran or control
o Kovacs, 2001, two weeks each diet: Breakfast replaced with solid meal or semi-solid meal with or without fiber supplement; 6.6g per day guar gum
o Meada, 2005, 12 weeks: Reduced calorie diet (Output, 400kcal) plus fiber supplement; 4.5g agar
o Vuksan, 1999, three weeks: Two grams per 100kcal konjac mannan fiber or two grams per 100kcal wheat bran fiber.

Energy Intake

Six studies: One positive-rated randomized controlled trial (Rossner et al, 1987), two neutral-rated randomized controlled trials (Pasman and Westerterp-Plantenga et al, 1997; Rigaud et al, 1990), one negative-rated randomized controlled trial (Dudani et al, 1986), one positive-rated randomized controlled trial with crossover (Kovacs et al, 2001) and one neutral-rated randomized controlled trial with crossover (Pasman et al, 1997), investigated the impact of fiber supplements on energy intake in obese individuals.

Decreased Energy Intake

Two studies (Pasman, 1997; Rossner, 1987) found decreased energy intake with five grams to 40g fiber per day for one week to three months.

* Decreased energy intake
o Pasman, 1997, one week each (crossover): 40g per day guar gum; one week AND four mJ with 20g guar gum or control or six mJ with 20g guar gum or control
o Rossner, 1987, three months: 1,400-kcal diet with five grams per day fiber supplement (grain and citrus fiber) or placebo; two months AND 1,600-kcal diet with seven grams per day fiber supplement (vegetable, grain and citrus fiber) or placebo.

No Difference in Energy Intake

Three studies (Kovacs, 2001; Pasman and Westerterp-Plantenga, 1997; Rigaud, 1990) found no difference in energy intake in individuals that consumed 6.6g to 20g fiber supplements for two weeks to 14 months.

* No difference in energy intake
o Kovacs, 2001, two weeks each diet: Breakfast replaced with solid meal or semi-solid meal with or without fiber supplement; 6.6g per day guar gum
o Pasman and Westerterp-Plantenga, 1997, 14 months: 16g to 20g guar gum, 10g to 15g guar gum or control
o Rigaud, 1990, six months: Seven grams per day insoluble fiber supplement (beet, barley, citrus; 90% insoluble) or placebo.

Satiety and Hunger

Eight studies: Two positive-rated randomized controlled trials (Rossner et al, 1987; Ryttig et al, 1989), three neutral-rated randomized controlled trials (Hylander et al, 1983; Pasman and Westerterp-Plantenga et al, 1997; Rigaud et al, 1990) and two positive-rated randomized controlled trials with crossover (Adam et al, 2005; Kovacs et al, 2001) and one neutral-rated randomized controlled trial with crossover (Pasman et al, 1997), explored the impact of fiber supplements on hunger in obese individuals.

Less Hunger

Five studies (Hylander, 1983; Kovacs, 2001; Pasman and Westerterp-Plantenga, 1997; Rigaud, 1990; Ryttig, 1989) found significantly less hunger or increased satiety, following consumption of fiber supplements providing six grams to 20g fiber for two weeks to 14 months.

* Less hunger or greater satiety with fiber supplements
o Hylander, 1983, three weeks: 6.6g ispaghula, 6.6g bran or control
o Kovacs, 2001, two weeks each diet: Breakfast replaced with solid meal or semi-solid meal with or without fiber supplement; 6.6g per day guar gum
o Pasman and Westerterp-Plantenga, 1997, 14 months: 16g to 20g guar gum, 10g to 15g guar gum or control
o Rigaud, 1990, six months: Seven grams per day insoluble fiber supplement (beet, barley, citrus; 90% insoluble) or placebo
o Ryttig, 1989: 1,200-kcal diet with seven grams per day fiber supplement or placebo for 11 weeks, then 1,600-kcal diet with six grams per day fiber supplement or placebo for 16 weeks, then ad lib diet with six grams per day fiber supplement for 25 weeks.

No Impact on Hunger

Three studies (Adam, 2005; Pasman, 1997; Rossner, 1987) found that fiber supplements providing five grams to 40g fiber for one meal to three months had no impact on satiety or hunger in obese individuals.

* No change between groups in hunger or satiety with fiber supplements
o Adam, 2005, one meal: 50g galactose with 2.5g guar gum or control at breakfast
o Pasman, 1997, one week each (crossover): 40g per day guar gum; one week AND four mJ with 20g guar gum or control or six mJ with 20g guar gum or control
o Rossner, 1987, three months: 1,400-kcal diet with five grams per day fiber supplement (grain and citrus fiber) or placebo; two months AND 1,600-kcal diet with seven grams per day fiber supplement (vegetable, grain and citrus fiber) or placebo.

Adam also explored the impact of fiber supplements on Glucagon-like peptide 1 (GLP-1), a gastrointestinal peptide believed to signal satiety via gastric and small bowel nerves. GLP-1 was found to be elevated with administration of 50g galactose and 2.5g guar gum, however the increase in GLP-1 was not related to ratings of satiety in obese individuals, as was seen in normal-weight individuals.

Serum Lipids

Five studies: Three neutral-rated randomized controlled trials (Birketvedt et al, 2000; Pasman and Westerterp-Plantenga et al, 1997; Solum et al, 1987) and two positive-rated randomized controlled trials with crossover (Meada et al, 2005; Vuksan et al, 1999), examined the impact of fiber supplements on serum lipids in overweight and obese individuals.

No Difference in Change in Serum Lipids

The majority of studies (Birketvedt, 2000; Pasman and Westerterp-Plantenga, 1997; Solum, 1987; Vuksan, 1999) found no difference in the change in serum lipids from control with fiber supplementation on primarily hypocaloric diets.

Improved Total Cholesterol

One study found greater improvement in total cholesterol in the group which consumed 4.5g fiber from agar for 12 weeks.

* Decreased serum lipids with fiber supplements
o Meada, 2005, 12 weeks: Reduced calorie diet (Output -400kcal) plus fiber supplement; 4.5g agar.
* No change between groups in serum lipids with fiber supplements
o Birketvedt, 2000, 24 weeks: 1,200-kcal diet (15g per day dietary fiber) plus fiber supplement (grain and citrus fiber; 85% insoluble) or control; Weeks One to Eight, six grams per day; Weeks Nine to 24, four grams per day
o Pasman and Westerterp-Plantenga, 1997, 14 months: 16g to 20g guar gum, 10g to 15g guar gum or control
o Solum, 1987, 12 weeks: 1,200-kcal diet (25g per day dietary fiber) with six grams per day fiber supplement (grain and citrus fiber) or control
o Vuksan, 1999, three weeks: Two grams per 100kcal konjac mannan fiber or two grams per 100kcal wheat bran fiber.

Blood Pressure

Seven studies: Two positive-rated randomized controlled trials (Rossner et al, 1987; Ryttig et al, 1989), two neutral-rated randomized controlled trials (Rigaud et al, 1990; Solum et al, 1987) and three positive-rated randomized controlled trials with crossover (Kovacs et al, 2001; Meada et al, 2005; Vuksan et al, 1999), examined and explored the impact of fiber supplements on blood pressure in overweight and obese individuals.

Decrease in Diastolic Blood Pressure

Two studies (Rossner, 1987, Ryttig, 1989) found a decrease in diastolic blood pressure (DBP) with seven to 26g dietary fiber for three to 12 months. Solum (1987) and Vuksan, 1999, found a decrease in blood pressure with six to 14g fiber for three to 12 weeks.

* Decreased blood pressure with fiber supplements
o Rossner, 1987, three months: 1,400-kcal diet with five grams per day fiber supplement (grain and citrus fiber) or placebo; two months AND 1,600-kcal diet with seven grams per day fiber supplement (vegetable, grain and citrus fiber) or placebo
o Ryttig, 1989: 1,200-kcal diet with seven grams per day fiber supplement or placebo for 11 weeks, then 1,600-kcal diet with six grams per day fiber supplement or placebo for 16 weeks, then ad lib diet with six grams per day fiber supplement for 25 weeks
o Solum, 1987, 12 weeks: 1,200-kcal diet (25g per day dietary fiber) with six grams per day fiber supplement (grain and citrus fiber) or control
o Vuksan, 1999, three weeks: Two grams per 100kcal konjac mannan fiber or two grams per 100kcal wheat bran fiber.

No Difference

Three studies (Kovacs, 2001; Maeda, 2005; Rigaud, 1990) found 4.5 to seven grams dietary supplements, for two to 30 weeks, led to no difference in the change in blood pressure from control.

* No change between groups in blood pressure with fiber supplements
o Vuksan, 1999, two weeks each diet: Breakfast replaced with solid meal or semi-solid meal with or without fiber supplement; 6.6g per day guar gum
o Meada, 2005, 12 weeks: Reduced-calorie diet (Output -400kcal) plus fiber supplement; 4.5g agar
o Rigaud, 1990, six months: Seven grams per day insoluble fiber supplement (beet, barley, citrus; 90% insoluble) or placebo.

Serum Glucose:

Six studies: One neutral-rated randomized controlled trial (Pasman and Westerterp-Plantenga et al, 1997) and five positive-rated randomized controlled trials with crossover (Adam et al, 2005; Behall et al, 2005; Kovacs et al, 2001; Meada et al, 2005; Vuksan et al, 1999), examined the effect of fiber supplements on glucose levels in obese and overweight individuals. All studies found no difference in change in glucose from control with fiber supplementation on primarily hypocaloric diets.

* No change in serum glucose with fiber supplement
o Adam, 2005, one meal: 50g galactose with 2.5g guar gum or control at breakfast Behall, 2005, one meal (crossover): 3.23g B-glucan (oats), 12.1g B-glucan (barley) at breakfast Kovacs, 2001, two weeks each diet: Breakfast replaced with solid meal or semi-solid meal with or without fiber supplement; 6.6g per day guar gum Meada, 2005, 12 weeks: Reduced calorie diet (Output - 400kcal) plus fiber supplement; 4.5g agar Pasman and Westerterp-Plantenga, 1997, 14 months: 16g to 20g guar gum, 10g to 15g guar gum or control Vuksan, 1999, three weeks: Two grams per 100kcal konjac mannan fiber or two grams per 100kcal wheat bran fiber.

Do Cholesterol Drugs Do Any Good?

2010-10-16T19:07:00.000-05:00

Do Cholesterol Drugs Do Any Good?

So how can anyone question the benefits of such a drug?

For one thing, many researchers harbor doubts about the need to drive down cholesterol levels in the first place. Those doubts were strengthened on Jan. 14, when Merck and Schering-Plough (SGP) revealed results of a trial in which one popular cholesterol-lowering drug, a statin, was fortified by another, Zetia, which operates by a different mechanism. The combination did succeed in forcing down patients' cholesterol further than with just the statin alone. But even with two years of treatment, the further reductions brought no health benefit.
DOING THE MATH

The second crucial point is hiding in plain sight in Pfizer's own Lipitor newspaper ad. The dramatic 36% figure has an asterisk. Read the smaller type. It says: "That means in a large clinical study, 3% of patients taking a sugar pill or placebo had a heart attack compared to 2% of patients taking Lipitor."

Now do some simple math. The numbers in that sentence mean that for every 100 people in the trial, which lasted 3 1/3 years, three people on placebos and two people on Lipitor had heart attacks. The difference credited to the drug? One fewer heart attack per 100 people. So to spare one person a heart attack, 100 people had to take Lipitor for more than three years. The other 99 got no measurable benefit. Or to put it in terms of a little-known but useful statistic, the number needed to treat (or NNT) for one person to benefit is 100.

Compare that with, say, today's standard antibiotic therapy to eradicate ulcer-causing H. pylori stomach bacteria. The NNT is 1.1. Give the drugs to 11 people, and 10 will be cured.

A low NNT is the sort of effective response many patients expect from the drugs they take. When Wright and others explain to patients without prior heart disease that only 1 in 100 is likely to benefit from taking statins for years, most are astonished. Many, like Winn, choose to opt out.

Plus, there are reasons to believe the overall benefit for many patients is even less than what the NNT score of 100 suggests. That NNT was determined in an industry-sponsored trial using carefully selected patients with multiple risk factors, which include high blood pressure or smoking. In contrast, the only large clinical trial funded by the government, rather than companies, found no statistically significant benefit at all. And because clinical trials themselves suffer from potential biases, results claiming small benefits are always uncertain, says Dr. Nortin M. Hadler, professor of medicine at the University of North Carolina at Chapel Hill and a longtime drug industry critic. "Anything over an NNT of 50 is worse than a lottery ticket; there may be no winners," he argues. Several recent scientific papers peg the NNT for statins at 250 and up for lower-risk patients, even if they take it for five years or more. "What if you put 250 people in a room and told them they would each pay $1,000 a year for a drug they would have to take every day, that many would get diarrhea and muscle pain, and that 249 would have no benefit? And that they could do just as well by exercising? How many would take that?" asks drug industry critic Dr. Jerome R. Hoffman, professor of clinical medicine at the University of California at Los Angeles.

Carbohydrate nutrition and inflammatory disease mortality in older adults -- Buyken et al. 92 (3): 634 -- American Journal of Clinical Nutrition

2010-08-25T16:29:00.000-05:00

Carbohydrate nutrition and inflammatory disease mortality in older adults -- Buyken et al. 92 (3): 634 -- American Journal of Clinical Nutrition

Background: Several studies suggest that carbohydrate nutrition is related to oxidative stress and inflammatory markers.

Objective: We examined whether dietary glycemic index (GI), dietary fiber, and carbohydrate-containing food groups were associated with the mortality attributable to noncardiovascular, noncancer inflammatory disease in an older Australian cohort.

Conclusion: These data provide new epidemiologic evidence of a potentially important link between GI and inflammatory disease mortality among older women.

Too Much Sugar Is Bad, But Which Sugar Is Worse: Fructose Or Glucose?

2010-08-15T14:37:00.000-05:00

Too Much Sugar Is Bad, But Which Sugar Is Worse: Fructose Or Glucose?:

ScienceDaily (Apr. 25, 2009) — In 2005, the average American consumed 64kg of added sugar, a sizeable proportion of which came through drinking soft drinks. Now, in a 10-week study, Peter Havel and colleagues, at the University of California at Davis, Davis, have provided evidence that human consumption of fructose-sweetened but not glucose-sweetened beverages can adversely affect both sensitivity to the hormone insulin and how the body handles fats, creating medical conditions that increase susceptibility to heart attack and stroke."

In the study, overweight and obese individuals consumed glucose- or fructose-sweetened beverages that provided 25% of their energy requirements for 10 weeks. During this period, individuals in both groups put on about the same amount of weight, but only those consuming fructose-sweetened beverages exhibited an increase in intraabdominal fat.

Further, only these individuals became less sensitive to the hormone insulin (which controls glucose levels in the blood) and showed signs of dyslipidemia (increased levels of fat-soluble molecules known as lipids in the blood).

Fructose sugar makes maturing human fat cells fatter, less insulin-sensitive, study finds

2010-08-15T14:36:00.000-05:00

Fructose sugar makes maturing human fat cells fatter, less insulin-sensitive, study finds

Fructose Sugar Makes Maturing Human Fat Cells Fatter, Less Insulin-Sensitive, Study Finds

ScienceDaily (June 21, 2010) — Fructose, a sugar widely used in soft drinks and processed foods, often gets some of the blame for the widespread rise in obesity. Now a laboratory study has found that when fructose is present as children's fat cells mature, it makes more of these cells mature into fat cells in belly fat and less able to respond to insulin in both belly fat and fat located below the skin.

Cancer cells slurp up fructose, US study finds | Reuters

2010-08-06T10:52:00.000-05:00

Cancer cells slurp up fructose, US study finds | Reuters

Cancer cells slurp up fructose, US study finds

Mon Aug 2, 2010 5:20pm EDT

* Study shows fructose used differently from glucose

* Findings challenge common wisdom about sugars

WASHINGTON Aug 2 (Reuters) - Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same.

Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found.

They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types.

"These findings show that cancer cells can readily metabolize fructose to increase proliferation," Dr. Anthony Heaney of UCLA's Jonsson Cancer Center and colleagues wrote.

"They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth."

Americans take in large amounts of fructose, mainly in high fructose corn syrup, a mix of fructose and glucose that is used in soft drinks, bread and a range of other foods.

Politicians, regulators, health experts and the industry have debated whether high fructose corn syrup and other ingredients have been helping make Americans fatter and less healthy.

Okay, so here comes the "high fructose corn syrup is bad, let's tax/regulate it" brigade. The article continues with politicians and their anti-HFCS crusade.
Sugar is HALF FRUCTOSE
High fructose corn syrup is HALF FRUCTOSE
Fruits and vegetables are ALL FRUCTOSE
Breads and starches are glucose, which is also not good.
So no, fructose is not good, but the idea that therefore the government should tax it is stupid. Why? Well, the only reason we use HFCS is because the government taxes sugar, which is mostly made outside the US, to ENCOURAGE HFCS, which mostly comes from US corn. They also subsidize corn, big time. They also have tricked us into thinking a high carb diet is good for use, so they can sell more US corn, wheat, and soy, all of which are bad for us. And they have demonized animal products and ignored the science which continually proves them wrong. Finally, they say this tax on HFCS will go to help treat illnesses caused by HFCS. NO IT WILL NOT. When the government sued the tobacco companies, how much of that went to sick people? NONE. The government spent every penny of it. Too bad they didn't keep some, for economic crises like the one we're in now.

At the very least, let this article be a lesson on how poorly the gov. does science. In Germany low carb diets are used to treat cancer, but in the US we're told this is ridiculous. Who's laughing now? Diabetics are told by the gov. to eat plenty of fructose, which doesn't raise blood sugar. Oh well, guess cancer is okay now? Is Michelle Obama going to stop encouraging us to eat tons of fruit/fructose every day? Probably not. Doesn't really matter, since the government's new "food safety modernization act" is going to destroy all the small farms and farmer's markets.

Feds admit storing checkpoint body scan images | Privacy Inc. - CNET News

2010-08-04T23:59:00.000-05:00

Feds admit storing checkpoint body scan images | Privacy Inc. - CNET News

For the last few years, federal agencies have defended body scanning by insisting that all images will be discarded as soon as they're viewed. The Transportation Security Administration claimed last summer, for instance, that "scanned images cannot be stored or recorded."

Now it turns out that some police agencies are storing the controversial images after all. The U.S. Marshals Service admitted this week that it had surreptitiously saved tens of thousands of images recorded with a millimeter wave system at the security checkpoint of a single Florida courthouse.

This follows an earlier disclosure (PDF) by the TSA that it requires all airport body scanners it purchases to be able to store and transmit images for "testing, training, and evaluation purposes." The agency says, however, that those capabilities are not normally activated when the devices are installed at airports.

Body scanners penetrate clothing to provide a highly detailed image so accurate that critics have likened it to a virtual strip search. Technologies vary, with millimeter wave systems capturing fuzzier images, and backscatter X-ray machines able to show precise anatomical detail. The U.S. government likes the idea because body scanners can detect concealed weapons better than traditional magnetometers.

This privacy debate, which has been simmering since the days of the Bush administration, came to a boil two weeks ago when Homeland Security Secretary Janet Napolitano announced that scanners would soon appear at virtually every major airport. The updated list includes airports in New York City, Dallas, Washington, Miami, San Francisco, Seattle, and Philadelphia.

The Electronic Privacy Information Center, a Washington, D.C.-based advocacy group, has filed a lawsuit asking a federal judge to grant an immediate injunction pulling the plug on TSA's body scanning program. In a separate lawsuit, EPIC obtained a letter (PDF) from the Marshals Service, part of the Justice Department, and released it on Tuesday afternoon.

These "devices are designed and deployed in a way that allows the images to be routinely stored and recorded, which is exactly what the Marshals Service is doing," EPIC executive director Marc Rotenberg told CNET. "We think it's significant."

N Dakota, Alaska lead US job creation, study says | Reuters

2010-07-28T12:52:00.000-05:00

N Dakota, Alaska lead US job creation, study says | Reuters: "* Forty states have fewer jobs now than five years ago

* Bottom-ranking Nevada topped the jobs list in 2005

By Ellen Wulfhorst

NEW YORK, July 26 (Reuters) - North Dakota and Alaska have added the most jobs, while Nevada, California and Florida have lost the most, in the last five years, according to research released on Monday."

[...]

North Dakota and other states that added jobs did not undergo the economic volatility of recent years as much as other states, said G. Scott Thomas, a Portfolio.com demographer.

"There was no real estate boom or bubble and, as a result, they kept plodding along," Thomas said. "Now those numbers look fantastic."

Nevada ranked at the bottom of the list, having lost 113,000 jobs in the last five years, followed by California and Florida, it said.

That marked a dramatic change in fortunes for Nevada and Florida, which finished first and second in jobs in a similar 2005 study, it said.

The change illustrates how little can be divined from such data, Thomas said.

"Five years ago, we said Nevada was No. 1, and now it's dead last," he said. "It does make you leery of economic forecasts."

No, it shows you that an artificially stoked boom will lead inevitably to a bust. The bigger the boom, the bigger the bust. So, cash for clunkers caused a small boom and bust. Now, how's Obama's stimulus coming along? With bank stocks soaring now, I predict bust in 5...4...3...

Together, Nevada, California and Florida have lost 1.69 million jobs since 2005, the study said.

Overall, the United States lost 4.51 million private-sector jobs from mid-2005 to mid-2010, it said. The study used U.S. Bureau of Labor Statistics data from the 50 U.S. states and the District of Columbia.

Other states at the bottom of the list were Michigan, Rhode Island, Georgia, Ohio and Arizona. The declines were a combination of real-estate problems, slowed construction and tourism and a drop in manufacturing, it said.

Eating high glycemic index foods may put women at higher risk for heart disease | Booster Shots | Los Angeles Times

2010-04-14T19:05:00.000-05:00

Eating high glycemic index foods may put women at higher risk for heart disease | Booster Shots | Los Angeles Times

All carbohydrates are not created equal, at least when it comes to heart disease. A new study released today finds that carbs with a high glycemic index--those that spike blood glucose levels quickly--may be linked with a higher risk of coronary heart disease in women.

[...]

Foods were analyzed to determine their glycemic index and glycemic load. The glycemic index measures how carbs effect blood sugar levels. High glycemic index foods are quickly digested and release glucose quickly into the bloodstream, making glucose levels jump. High-glycemic index foods include baked potatoes, watermelon and rice. Low glycemic index foods slowly release glucose into the bloodstream, keeping blood glucose levels more steady. Those foods include most fruits and vegetables, plus pasta and milk. Glycemic load refers to a food's ranking according to how many total grams of carbohydrate it has along with its glycemic index, and is found using a formula.

Other studies have found that high-carb diets increase triglycerides and lower HDL ("good") cholesterol levels as well as boosting blood glucose and insulin.

The Italian researchers discovered that the 25% of the women who ate the most amount of carbs had about twice the risk of heart disease as the 25% who ate the least amount of carbs. In terms of quality versus quantity carbs, quality won out: eating more high-glycemic index foods was more strongly linked with a greater risk of coronary heart disease than eating low-glycemic index foods. In the study, the authors wrote, "a high consumption of carbohydrates from high-glycemic index foods, rather than the overall quantity of carbohydrates consumed, appears to influence the risk of developing coronary heart disease."

Low Bone Mass in Subjects on a Long-term Raw Vegetarian Diet

2010-04-14T19:03:00.000-05:00

Arch Intern Med -- Abstract: Low Bone Mass in Subjects on a Long-term Raw Vegetarian Diet, March 28, 2005, Fontana et al. 165 (6): 684

Low Bone Mass in Subjects on a Long-term Raw Vegetarian Diet

Luigi Fontana, MD, PhD; Jennifer L. Shew, BS; John O. Holloszy, MD; Dennis T. Villareal, MD

Arch Intern Med. 2005;165:684-689.

Background Little is known regarding the health effects of a raw food (RF) vegetarian diet.

Methods We performed a cross-sectional study on 18 volunteers (mean ± SD age, 54.2 ± 11.5 years; male/female ratio, 11:7) on a RF vegetarian diet for a mean of 3.6 years and a comparison age- and sex-matched group eating typical American diets. We measured body composition, bone mineral content and density, bone turnover markers (C-telopeptide of type I collagen and bone-specific alkaline phosphatase), C-reactive protein, 25-hydroxyvitamin D, insulin-like growth factor 1, and leptin in serum.

Results The RF vegetarians had a mean ± SD body mass index (calculated as weight in kilograms divided by the square of height in meters) of 20.5 ± 2.3, compared with 25.4 ± 3.3 in the control subjects. The mean bone mineral content and density of the lumbar spine (P= .003 and P<.001, respectively) and hip (P = .01 and P<.001, respectively) were lower in the RF group than in the control group. Serum C-telopeptide of type I collagen and bone-specific alkaline phosphatase levels were similar between the groups, while the mean 25-hydroxyvitamin D concentration was higher in the RF group than in the control group (P<.001). The mean serum C-reactive protein (P = .03), insulinlike growth factor 1 (P = .002), and leptin (P = .005) were lower in the RF group.

Conclusion A RF vegetarian diet is associated with low bone mass at clinically important skeletal regions but is without evidence of increased bone turnover or impaired vitamin D status.

Does poverty make people obese, or is it the other way around? - By Daniel Engber - Slate Magazine

2010-03-29T14:08:00.000-05:00

Does poverty make people obese, or is it the other way around? - By Daniel Engber - Slate Magazine

Sociologists describe these patterns in terms of social gradients. The "health-wealth gradient" refers to the fact that, as a general rule, the richer you are, the healthier you are. This applies across different countries and across the full range of social classes within the same country. (It's not just that the very poorest people are sick.) No one knows exactly what causes the health-wealth gradient or why it's so resilient. It may be that rich people have access to better health care. Or, as we've seen, it could be that being sick costs you money. Then there's the possibility that poor people have a greater incentive to behave in unhealthy ways: Since they don't have as much money to spend on happiness, they "spend" their health instead. (The pleasures of smoking and eating, for example, are easy on the wallet and hard on the body.)

ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome

2010-03-28T13:18:00.000-05:00

ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome

Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome
Purchase the full-text article

References and further reading may be available for this article. To view references and further reading you must purchase this article.

T. Al-Sarraja, H. Saadic, J.S. Volekb and M.L. Fernandeza, Corresponding Author Contact Information

aDepartment of Nutritional Sciences, University of Connecticut, 3624 Horsebarn Road Ext, U 4017, Storrs, CT 06269, USA

bDepartment of Internal Medicine, United Arab Emirate University, Al-Ain, United Arab Emirates

cDepartment of Kinesiology, University of Connecticut, Storrs, CT 06269, USA
Received 10 March 2009;
revised 4 June 2009;
accepted 8 June 2009.
Available online 12 September 2009.

Abstract
Background and aims

Carbohydrate restriction (CR) has been shown to improve dyslipidemias associated with metabolic syndrome (MetS). We evaluated the effects of CR on lipoprotein subfractions and apolipoproteins in Emirati adults classified with the MetS.
Methods and results

39 subjects (15 men/24 women) were randomly allocated to a CR diet [20–25% energy from carbohydrate (CHO)] for 12 wk (CRD group) or a combination treatment consisting of CRD for 6 wk followed by the American Heart Association diet (50–55% CHO, AHA group) for an additional 6 wk. All subjects reduced body weight, LDL cholesterol and triglycerides (P < 0.01). At baseline all subjects had low concentrations of medium VLDL and total HDL particles associated with the very low plasma triglycerides and HDL cholesterol in this population. After 12 wk, the large VLDL subfraction was decreased over time for subjects in the CRD group (P < 0.01) while these changes were not observed in those subjects who changed to the AHA diet. The number of medium and small LDL particles decreased for all subjects rendering a less atherogenic lipoprotein profile. In agreement with these results, a significant decrease in apolipoprotein (apo) B was observed (P < 0.01). The medium HDL subfraction and apo A-II, which can be considered pro-atherogenic, were also decreased over time in the CRD group only.
Conclusions

These results suggest that weight loss favorably affects lipoprotein metabolism and that the Carbohydrate restricted diet had a better effect on atherogenic VLDL and HDL than the low fat diet recommended by AHA.

Keywords: Lipoprotein subfractions; Apolipoproteins; Carbohydrate restriction; Metabolic syndrome; United Arab Emirates

Fruits, vegetables and coronary heart disease : Abstract : Nature Reviews Cardiology

2010-03-28T13:16:00.001-05:00

Fruits, vegetables and coronary heart disease : Abstract : Nature Reviews Cardiology

Fruits, vegetables and coronary heart disease

See also: Correspondence by Ghayur & Janssen

Luc Dauchet1, Philippe Amouyel1 & Jean Dallongeville1 About the authors
Top of page
Abstract

Diet plays an important part in the maintenance of optimal cardiovascular health. This Review summarizes the evidence for a relationship between fruit and vegetable consumption and the occurrence of coronary heart disease. This evidence is based on observational cohort studies, nutrition prevention trials with fruit and vegetables, and investigations of the effects of fruit and vegetables on cardiovascular risk factors. Most of the evidence supporting a cardioprotective effect comes from observational epidemiological studies; these studies have reported either weak or nonsignificant associations. Controlled nutritional prevention trials are scarce and the existing data do not show any clear protective effects of fruit and vegetables on coronary heart disease. Under rigorously controlled experimental conditions, fruit and vegetable consumption is associated with a decrease in blood pressure, which is an important cardiovascular risk factor. However, the effects of fruit and vegetable consumption on plasma lipid levels, diabetes, and body weight have not yet been thoroughly explored. Finally, the hypothesis that nutrients in fruit and vegetables have a protective role in reducing the formation of atherosclerotic plaques and preventing complications of atherosclerosis has not been tested in prevention trials. Evidence that fruit and vegetable consumption reduces the risk of cardiovascular disease remains scarce thus far.

Very interesting. I'm sure vegetables have good properties, but I'm always astounded at the way people make vegetables into a magical food, and demonize meat. There's a guy out there with a blog who basically says eating veges make you "cancer proof". I prefer to look at the evidence, and the evidence that I've seen for eating veges is all observational. This presents a problem. People who eat veges are people usually who care about their health. They are more likely to exercise, take vitamins, eat less sugar, smoke less, sleep better, and be wealthier. All of those things are associated with increased health. This is called a confounding factor, and it is the reason why epidemiological or observational studies or surveys don't prove anything. You need a randomized, double blind, crossover study, but these, unfortunately, are very expensive.

"Change or Die," the Book, and Resolutions | The Fast Company Blog | Fast Company

2010-02-22T09:57:00.000-06:00

"Change or Die," the Book, and Resolutions | The Fast Company Blog | Fast Company

Of course, any kind of profound change is very challenging. The fact that got me started on this two-year project was that 90 percent of patients with severe heart disease fail to change their unhealthy lifestyles even after their doctors tell them that they're in a "change or die" situation.

What can we do to improve the odds and make those New Years resolutions stick?

Start by realizing that it's hard to do away with our "problems" when those "problems" are actually our attempted "solutions" to deeper issues. For example, you might think that overeating is your problem, and so your New Years resolution is to go on a diet and lose weight. But what if overeating is the way you try to solve more fundamental problems such as stress, anxiety, loneliness, and existential despair? Overeating is an "attempted solution" to those deeper troubles. It's a bad solution, because ultimately it can undermine or ruin your health. But it's the "solution" that you know and trust.

In this case the way to change is to find other, better solutions to the underlying problems of stress, anxiety, and loneliness. Instead of going on a diet, you might want to take up yoga or meditation, or to get more involved in a social group or church. Instead of going back to the same "solution" that has failed you year after year when you make New Years resolutions--in this case, dieting--why not try a new solution?

The paradox, of course, is that these new solutions don't occur to us because of how we've framed the problem to begin with.

If you're interested in looking further into these issues, please pick up a copy of my new book "Change or Die: The Three Keys to Change at Work and in Life." I also strongly recommend the writings of Dr. Richard Fisch, a pioneering psychologist. Fisch hit upon this fascinating approach of reframing problems and solutions back in the 1960s along with his colleagues at the Brief Therapy Center in Palo Alto, where he still practices.

Protective Role of Vitamin D on the Cardiovascular System

2010-02-20T18:57:00.000-06:00

USPharmacist.com; Protective Role of Vitamin D on the Cardiovascular System

Heart disease is a broad term that describes a range of diseases that affect the cardiovascular system and result in approximately 630,000 deaths annually in the United States.1 Cardiovascular disease (CVD) is the leading cause of death of both men and women above the age of 35 among all racial and ethnic groups.2 While risk factors such as increased age, male gender, and family history are nonmodifiable, others, such as smoking, high cholesterol, hypertension, physical inactivity, obesity, diabetes mellitus, and stress are preventable.2 Another possible modifiable risk factor, vitamin D deficiency, has been identified and has caused debates in the literature as the protective role of vitamin D on the cardiovascular system continues to be investigated. This article will expand on this proposed phenomenon, providing deeper insight into recently published literature, as well as discuss the pharmacist’s role in preventing vitamin D deficiency.

Vitamin D: The Basics

Vitamin D refers to two biologically inactive precursors: vitamin D3 (cholecalciferol), produced mainly in the skin post exposure to ultraviolet (UV) radiation, and vitamin D2 (ergocalciferol), produced exogenously and entering the circulation solely after gastrointestinal absorption.3 Both vitamin D2 and D3 require hydroxylation reactions in the liver and kidney, closely regulated by the parathyroid hormone (PTH), to form the biologically active metabolite of vitamin D, 1,25(OH)2D (calcitriol).4 Vitamin D status is best measured by 25(OH)D concentrations or levels and not calcitriol levels for several reasons, including longer half-life (~3 weeks compared to ~8 hours for calcitriol), higher circulating serum concentrations, and tight regulation of calcitriol by PTH, resulting in falsely elevated calcitriol levels despite vitamin D deficiency.5 Currently, there is no universally accepted “normal” measure of 25(OH)D levels; however, it has been suggested that concentrations above 30 ng/mL are associated with decreased fracture rates and maximal parathyroid suppression.6

Although the classic function of vitamin D has been to increase the intestinal absorption of calcium for proper bone health, its role in health maintenance is beginning to expand with the finding of vitamin D receptors (VDRs) in many cells throughout the body, including cardiomyocytes, vascular smooth muscle, and endothelium.5,7 Additionally, recent studies have found that individuals with vitamin D deficiency have increased incidence of CVD.7

Article mentions Vitamin D and its effects on:
Atherosclerosis and Inflammation
Hypertension
Diabetes and Metabolic Syndrome

Movement comes with appetite: Insulin supresses orexin

2010-02-15T14:17:00.001-06:00

domain-b.com : Healthy eating: Movement comes with appetite:

A body that is provided with food too often gets caught up in the maelstrom of a lack of exercise, obesity and ultimately diabetes. The trigger is a molecular switch that is controlled by insulin, a new study by scientists from ETH Zurich has revealed.

[...]

The key switch player in this is a transcription factor called Foxa2. Transcription factors are proteins that make sure other genes are activated and converted into proteins.

Foxa2 is found in the liver, where it influences fat-burning, but also in two important neuron populations in the hypothalamus - the region of the brain that controls the daily rhythm, sleep, intake of food and sexual behavior. The control element for Foxa2 activity is insulin, in both the liver and the hypothalamus.

If a person or animal ingests food, the beta cells in the pancreas release insulin, which blocks Foxa2. When fasting, there is a lack of insulin and Foxa2 is active. In the brain, the scientists have discovered, Foxa2 assists the formation of two proteins: MCH and orexin.

[...]

These two brain messenger substances trigger different behaviour patterns: the intake of food and spontaneous movement. If mammals are hungry, they are more alert and physically active. In short, they hunt and look for food. "If you watch a cat or a dog before feeding it, you can see this very clearly", says Stoffel.

Explanation found for lack of movement
The researchers discovered a disorder in obese mice: in these animals, Foxa2 is permanently active, regardless of whether the animals are fasting or full. This explains a well-known but until now unaccountable phenomenon: the lack of movement in obese people and animals.

To prove this, the researchers used a genetic trick to breed mice, in the brains of which Foxa2 is always active, regardless of whether they have just eaten or are fasting.

These mice produce more MCH and orexin and move five times more than normal animals, in which insulin deactivates Foxa2 after eating or which are obese. The genetically modified mice lose fatty tissue and form larger muscles. Their sugar and fat metabolism works flat out and their blood values are considerably improved.

Three meals a day suffice
For Stoffel, the study clearly shows that, "The body needs fasting periods to stay healthy." Moreover, you should make sure you have a good body weight. He therefore doesn't think much of eating many little meals spread out over the day; it is better to eat less frequently but well, and leave room in between to get hungry.

After all, because insulin is released during every meal, thus suppressing Foxa2, the motivation to do physical exercise and burn sugar and fat visibly decreases.

(Original: Silva JP, von Meyenn F, Howell J, Thorens B, Wolfrum C, Stoffel M. "Regulation of adaptive behaviour during fasting by hypothalamic Foxa2". Nature. Epub 2009 December 3, doi: 10.1038/nature08589."

Magnesium and inflammation | The Blog of Michael R. Eades, M.D.

2010-02-10T08:48:00.001-06:00

Magnesium and inflammation | The Blog of Michael R. Eades, M.D.

As the inflammatory hypothesis becomes more accepted, more and more physicians will be checking C-reactive protein levelsâ€”along with a few other inflammatory yardsticksâ€”to determine the inflammatory status of their patients. If the C-reactive protein level is found to be elevated, then steps can be taken, not just to reduce the C-reactive protein, but to treat the underlying inflammation so that the C-reactive proteinâ€”a marker of this underlying inflammationâ€”will normalize.

One easy step in the inflammation reduction process is to make sure magnesium intake is high.

The most recent issue of the Journal of the American College of Nutrition contains an article showing that as consumption of magnesium fell, the levels of C-reactive protein went up.

The paper points out that the majority of adults in the US (68%) don’t consume even the RDA of magnesium, which is, as far as I’m concerned, woefully low. Magnesium is an unbelievably important mineral for all sorts of body processes. Some 300+ enzymes use magnesium as a cofactor; magnesium helps regulate potassium status; magnesium acts as nature’s own calcium channel blocker, helping blood pressure stay down and blood vessels stay pliable; magnesium builds bones; magnesium is anti-inflammatory. The list of magnesium’s virtues goes on and on.

In fact, there exists an entire school of thought that posits that the entire Metabolic Syndrome is nothing but a manifestation of a a magnesium deficiency. Which isn’t as crazy as it sounds since virtually all the components of the Metabolic Syndromeâ€”diabetes, high blood pressure, obesity and lipid disordersâ€”are associated with low magnesium.

Why are so many people deficient in magnesium? Because there are no single foods that contain huge amounts of magnesium, and because there is no single food containing large amounts, there is no magnesium lobby. Look at calcium. Thanks to the dairy industry, we are constantly told that we need to get enough calcium, and we’re told right where we can get it. Milk and cheese. Same with vitamin C. The orange juice people never let us forget. Not so with magnesium, so no one really thinks of it.

[...]

Magnesium is just about our favorite supplement. In fact, if we just had one supplement to recommend, and no other, it would be magnesium. Take it at bedtime because it helps you sleep.

Features of a successful therapeutic fast of 382 days' duration

2010-02-09T10:28:00.001-06:00

Features of a successful therapeutic fast of 382 days' duration

Features of a successful therapeutic fast of 382 days' duration. Man fasted and loses 276 lbs.

Internet generation at risk of rickets: study

2010-01-23T16:01:00.001-06:00

Internet generation at risk of rickets: study

Bone-bending rickets can now be added to the list of ills linked to children spending uncounted hours before a computer screen, British researchers said Friday.

Youngsters with rickets, caused primarily by a chronic lack of vitamin D, develop painful and deformed bow-legs that do not grow properly.

The condition is linked mainly with extreme poverty and the 19th-century Victorian England of Charles Dickens, and can be easily avoided through a balanced diet and exposure to sunlight.

But doctors reported this month that cases of the debilitating disease have once again become "disconcertingly common" in Britain.

"Kids tend to stay indoors more these days and play on their computers instead of enjoying the fresh air," said Simon Pearce, a professor at Newcastle University in northeast England and lead author of a new study on Vitamin D deficiency.

"This means their vitamin D levels are worse than in previous years," he said in a press release.

Half of all adults in Britain -- especially in the north -- have Vitamin D deficiency in winter and spring, with one-in-six having severe deficiency.

The condition has been linked to cardiovascular disease, type 2 diabetes, several kinds of cancer and a soft-bone condition in adults called osteomalacia.

'U' Study: Vitamin D May Be Tied To Weight Loss - wcco.com

2009-12-21T21:44:00.001-06:00

'U' Study: Vitamin D May Be Tied To Weight Loss - wcco.com:

"A University of Minnesota study has found that higher levels of vitamin D on low-calorie diet may help people lose more weight, especially around the abdomen.

Researcher Shalamar Sibley, M.D., headed the study that measured 38 overweight men and women participants who had insufficient vitamin D levels. The participants were monitored for 11 weeks while on diet programs that contained 750 calories fewer than their estimated daily needs.

The study found that the subjects lost a quarter to a half pound more fat when their vitamin D level was increased."

Fat Head More On Alzheimer’s

2009-12-16T08:31:00.001-06:00

Fat Head More On Alzheimer’s

First, statins: If you want to delve into the chemistry of how statins affect brain function, you can read this article. In the meantime, here are a few highlights:

There is a clear reason why statins would promote Alzheimer’s. They cripple the liver’s ability to synthesize cholesterol, and as a consequence the level of LDL in the blood plummets. Cholesterol plays a crucial role in the brain, both in terms of enabling signal transport across the synapse and in terms of encouraging the growth of neurons through healthy development of the myelin sheath. Nonetheless, the statin industry proudly boasts that statins are effective at interfering with cholesterol production in the brain as well as in the liver.

Researchers are only recently discovering that both fat and cholesterol are severely deficient in the Alzheimer’s brain. It turns out that fat and cholesterol are both vital nutrients in the brain. The brain contains only 2% of the body’s mass, but 25% of the total cholesterol. Cholesterol is essential both in transmitting nerve signals and in fighting off infections.

[...]

The bottom line: your body makes cholesterol for a reason. Beat down your cholesterol with a drug, and you’re messing with your biochemistry at the cellular level. Not a good idea.

Of course, plenty of people who don’t take statins develop Alzheimer’s as well. I doubt statins are a major cause of the disease. But insulin resistance could be.

As Gary Taubes explains in Good Calories, Bad Calories, since neurons in the brain ideally last for a lifetime, they may be prime candidates for the accumulation of advanced glycation end-products, or AGEs — proteins linked haphazardly with sugars. (The acronym is convenient if not intentional; AGEs literally age your tissues.) AGEs appear to be involved in the early stages of the amyloid plaques that form in the brain. That means the foods that spike your blood sugar are already causing trouble. As an article on AGEs and diabetes explains:

A lowered glucose concentration will unhook the sugars from the amino groups to which they are attached; conversely, high glucose concentrations will have the opposite effect, if persistent.

And of course, when you spike your blood sugar, your body spikes its insulin output in response. If you become insulin resistant, your insulin will be high all the time — which in turn inhibits your brain’s ability to clear away plaques. As Gary Taubes wrote:

Insulin (in a test tube) will monopolize the attention of insulin-degrading enzyme (IDE), which normally degrades and clears both amyloid proteins and insulin from around the neurons. The more insulin available in the brain, by this scenario, the less IDE is available to clean up the amyloid, which then accumulates excessively and clumps into plaques … Mice that lack the gene to produce IDE develop version of both Alzheimer’s disease and Type 2 diabetes.

Good article from the creator of the movie Fathead on how cholesterol is good for the brain and carbs are bad. Highly recommend his movie, by the way. You can see some clips on youtube.com- search for fathead movie

Choline: an essential nutrient for public health. Steven H Zeisel. 2009; Nutrition Reviews - Wiley InterScience

2009-12-01T21:05:00.002-06:00

Choline: an essential nutrient for public health. Steven H Zeisel. 2009; Nutrition Reviews - Wiley InterScience

Choline was officially recognized as an essential nutrient by the Institute of Medicine (IOM) in 1998. There is significant variation in the dietary requirement for choline that can be explained by common genetic polymorphisms. Because of its wide-ranging roles in human metabolism, from cell structure to neurotransmitter synthesis, choline-deficiency is now thought to have an impact on diseases such as liver disease, atherosclerosis, and, possibly, neurological disorders. Choline is found in a wide variety of foods. Eggs and meats are rich sources of choline in the North American diet, providing up to 430 milligrams per 100 grams. Mean choline intakes for older children, men, women, and pregnant women are far below the adequate intake level established by the IOM. Given the importance of choline in a wide range of critical functions in the human body, coupled with less-than-optimal intakes among the population, dietary guidance should be developed to encourage the intake of choline-rich foods.

New Link Discovered Between Insulin And Core Body Temperature

2009-11-24T14:03:00.001-06:00

New Link Discovered Between Insulin And Core Body Temperature

A team led by scientists at The Scripps Research Institute have discovered a direct link between insulin - a hormone long associated with metabolism and metabolic disorders such as diabetes - and core body temperature. While much research has been conducted on insulin since its discovery in the 1920s, this is the first time the hormone has been connected to the fundamental process of temperature regulation.

The paper was published recently in an advance, online issue of the journal Diabetes, a journal of the American Diabetes Association, and will appear in the January print edition of the publication.

The scientists found that when insulin was injected directly into a specific area of the brain in rodents, core body temperature rose, metabolism increased, and brown adipose (fat) tissue was activated to release heat. The research team also found that these effects were dose-dependent - up to a point, the more insulin, the more these metabolic measures rose.

"Scientists have known for many years that insulin is involved in glucose regulation in tissues outside the brain," said Scripps Research neurobiologist Manuel Sanchez-Alavez, who was first author of the new paper with Bartfai lab colleagues Iustin V. Tabarean and Olivia Osborn (now at the University of California, San Diego). "The connection to temperature regulation in the brain is new."

[...]

The authors note that while their new paper illuminates a key piece of the puzzle of the body's metabolic processes, it also raises many intriguing questions: How does insulin get to the brain's preoptic area - does it cross the blood-brain barrier or is it produced locally? Are diabetics, who are insensitive to insulin in peripheral tissues, still sensitive to insulin in the brain; if so, could this dichotomy be used in the development of a new therapy? Could scientists find a way to use these new insights to increase energy expenditure for the purpose of weight loss?

Very interesting. I have a low body temperature, so I wonder if there's a relationship between low body temps and pre-diabetes? I wonder if anyone has found that overweight people have lower body temps- kind of a sign of slow metabolism? Insulin resistance in the brain is also an interesting prospect because dopamine needs insulin to be utilized, and low dopamine causes ADD, and ADD and obesity are related conditions.

'Spoonful Of Sugar' Makes The Worms' Life Span Go Down

2009-11-08T01:58:00.002-06:00

Spoonful Of Sugar Makes The Worms Life Span Go Down

If worms are any indication, all the sugar in your diet could spell much more than obesity and type 2 diabetes. Researchers reporting in the November issue of Cell Metabolism, a Cell Press publication, say it might also be taking years off your life.

By adding just a small amount of glucose to C. elegans usual fare of straight bacteria, they found the worms lose about 20 percent of their usual life span. They trace the effect to insulin signals, which can block other life-extending molecular players.

Insulin’s Role in the Aging Body :: Scienceline

2009-11-06T14:30:00.001-06:00

Insulin’s Role in the Aging Body - Scienceline

Insulin, a hormone well known for its role in diabetes, may also lie at the root of another common but serious medical condition: age-related muscle loss, known as sarcopenia.

In fact, sarcopenia is in part due to muscle tissue not responding properly to insulin, according to a new study in the journal Diabetologia.

The researchers found that an increased dose of insulin restored the muscle-building processes that tend to deteriorate with old age. Unfortunately, insulin cannot be used as a treatment for sarcopenia due to its toxic effects in high concentrations. Still, the new results help clarify its role in muscle growth and could serve as a basis for future treatments. Sarcopenia affects 24 percent of adults between 45 and 70 years old, and half of people over 80.

“The new finding serves as a proof of concept,” said Elena Volpi, a researcher at the University of Texas Medical Branch at Galveston. “It confirms our belief that the age-related decline in muscle growth is a true case of insulin resistance, which is an important piece to the larger puzzle of treating sarcopenia.”

[...]

In type 2 diabetes, insulin resistance — a condition in which normal amounts of insulin fail to produce a typical insulin response in the body — prevents the body from storing sugar molecules in cells, eventually leading to high blood sugar. Test subjects in the Texas study, however, had normal blood sugar levels. This suggests the insulin resistance seen in elderly people is not a matter of sugar control.

Instead, the researchers believe insulin resistance seen in old age results from changes in blood flow. In addition to helping store sugar, insulin acts as a signal for the dilation of blood vessels to increase blood flow and deliver nutrients to muscle tissue. When capillaries fail to respond to these signals, blood flow slows down and muscle growth decreases.

Vitamin D May Improve Melanoma Survival HealthDay

2009-10-19T20:17:00.001-05:00

HealthDay Vitamin D May Improve Melanoma Survival

Vitamin D May Improve Melanoma Survival
But levels are too low in many Americans, researchers say

By Randy Dotinga
HealthDay Reporter

SATURDAY, Sept. 26 (HealthDay News) -- Higher levels of vitamin D are linked to less severe, less deadly melanoma lesions in people with skin cancer, new research suggests.

The findings provide more support for the idea that vitamin D is crucial to skin health. Many Americans, however, don't get enough of it, perhaps because they limit sun exposure and drink less milk than in the past.

"Although avoiding sunburn is very important in order to prevent melanoma, it is also important to avoid becoming deficient in vitamin D," said Dr. Julia A. Newton-Bishop, a dermatology professor at the University of Leeds in England and a study co-author. "This is especially important for melanoma patients in whom low vitamin D levels appear to be harmful."

Vegetarian diet bad for bone health - Journal Article

2009-10-19T20:08:00.001-05:00

SpringerLink - Journal Article

Abstract
Background A long-term vegetarian diet is generally poor in vitamin B group. The lack of vitamin B12 together with vitamin B6 and folate deficiency is closely related to homocysteine metabolism. Hyperhomocysteinemia was found to be associated with increased bone turnover markers and increased fracture risk. Thus, hyperhomocysteinemia, vitamin B12 and folate deficiency may be regarded as novel risk factors for micronutrient deficiency-related osteoporosis.
Aim of the study To assess the possible impact of a vegetarian diet on bone mineral density in cohort of Slovak vegetarian women.
Methods Fasting serum glucose, albumin, calcium, phosphorous and creatinine as well as bone markers, serum vitamin B12, folate and plasma levels of total homocysteine were assessed in two nutritional groups (vegetarians vs. nonvegetarians) of apparently healthy women (age range 20–70 years). Bone mineral density of the femoral neck, trochanter, total femur and lumbar spine was measured in all subjects.
Results Vegetarians had a significantly lower weight (p < 0.05), higher PTH (p < 0.01) and homocysteine (p < 0.001). Vitamin B12 was significantly higher in nonvegetarians (p < 0.001). No differences were observed in folate levels. Univariate analysis showed significant association between homocysteine and B12 (p < 0.01), folate (p < 0.001), creatinine (p < 0.001), total proteins (p < 0.049), age (p < 0.001) and vegetarian food intake (p < 0.001). Vegetarians had a significantly lower TrFBMD (p < 0.05) and ToFBMD (p < 0.05). Age and CTx were significant predictors in all sites of measured BMD and PTH. A strong correlation between homocysteine and FNBMD (r = −0.2009, p < 0.002), TrFBMD (r = −0.1810, p < 0.004) and ToFBMD (r = −0.2225, p < 0.001) was found in all subjects.
Conclusion Homocysteine is one of the predictors of bone mineral density, and hyperhomocysteinemia is associated with lower bone mineral density. In healthy adults, homocysteine levels are dependent on age as well as on nutritional habits. Thus, elderly women on a vegetarian diet seem to be at higher risk of osteoporosis development than nonvegetarian women.

Diets bad for the teeth are also bad for the body

2009-10-19T19:16:00.001-05:00

Diets bad for the teeth are also bad for the body

Diets bad for the teeth are also bad for the body
Beyond the immediate distress, dental pain may portend future medical problems

Dental disease may be a wake-up call that your diet is harming your body.

"The five-alarm fire bell of a tooth ache is difficult to ignore," says Dr. Philippe P. Hujoel, professor of dental public health sciences at the University of Washington (UW) School of Dentistry in Seattle. Beyond the immediate distress, dental pain may portend future medical problems. It may be a warning that the high-glycemic diet that led to dental problems in the short term may, in the long term, lead to potentially serious chronic diseases.

Hujoel reviewed the relationships between diet, dental disease, and chronic systemic illness in a report published July 1 in the Journal of Dental Research. He weighed two contradictory viewpoints on the role of dietary carbohydrates in health and disease. The debate surrounds fermentable carbohydates: foods that turn into simple sugars in the mouth. Fermentable carbohydrates are not just sweets like cookies, doughnuts, cake and candy. They also include bananas and several tropical fruits, sticky fruits like raisins and other dried fruits, and starchy foods like potatoes, refined wheat flour, yams, rice, pasta, pretzels, bread, and corn.

One viewpoint is that certain fermentable carbohydrates are beneficial to general health and that the harmful dental consequences of such a diet should be managed by the tools found in the oral hygiene section of drugstores. A contrasting viewpoint suggests that fermentable carbohydrates are bad for both dental and general health, and that both dental and general health need to be maintained by restricting fermentable carbohydrates.

The differing perspectives on the perceived role of dietary carbohydrates have resulted in opposing approaches to dental disease prevention, Hujoel notes, and have prompted debates in interpreting the link between dental diseases and such systemic diseases as obesity, diabetes, and some forms of cancer.

Over the past twenty years or so, Hujoel says, people have been advised to make fermentable dietary carbohydrates the foundation of their diet. Fats were considered the evil food. A high-carbohydrate diet was assumed to prevent a number of systemic chronic diseases. Unfortunately, such a diet - allegedly good for systemic health - was bad for dental health. As a result, cavities or gingival bleeding from fermentable carbohydrates could be avoided only – and not always successfully, as Hujoel points out -- by conscientious brushing, fluorides, and other types of dental preventive measures. When these measures are not successful, people end up with cavities and gum disease.

Hujoel observed that the dental harms of fermentable carbohydrates have been recognized by what looks like every major health organization. Even those fermentable carbohydrates assumed to be good for systemic health break down into simple sugars in the mouth and promote tooth decay. All fermentable carbohydrates have the potential to induce dental decay, Hujoel notes.

But what if fermentable carbohydrates are also bad for systemic health? Hujoel asks. What if dietary guidelines would start incorporating the slew of clinical trial results suggesting that a diet low in fermentable carbohydrates improves cardiovascular markers of disease and decreases body fat? Such a change in perspective on fermentable carbohydrates, and by extension, on people's diets, could have a significant impact on the dental profession, as a diet higher in fat and protein does not cause dental diseases, he notes. Dentists would no longer be pressed to recommend to patients diets that are bad for teeth or remain mum when it comes to dietary advice. Dentists often have been reluctant, Hujoel says, to challenge the prevailing thinking on nutrition. Advising patients to reduce the amount or frequency of fermentable carbohydrate consumption is difficult when official guidelines suggested the opposite.

The close correlation between the biological mechanisms that cause dental decay and the factors responsible for high average levels of glucose in the blood is intriguing. Hujoel explains that eating sugar or fermentable carbohydrates drops the acidity levels of dental plaque and is considered an initiating cause of dental decay.

"Eating these same foods, he says, is also associated with spikes in blood sugar levels. There is fascinating evidence that suggests that the higher the glycemic level of a food, the more it will drop the acidity of dental plaque, and the higher it will raise blood sugar. So, possibly, dental decay may really be a marker for the chronic high-glycemic diets that lead to both dental decay and chronic systemic diseases. This puts a whole new light on studies that have linked dental diseases to such diverse illnesses as Alzheimer's disease and pancreatic cancer."

The correlations between dental diseases and systemic disease, he adds, provide indirect support for those researchers who have suggested that Alzheimer's disease and pancreatic cancer are due to an abnormal blood glucose metabolism.

The hypotheses on dental diseases as a marker for the diseases of civilization were postulated back in the mid-20th century by two physicians: Thomas Cleave and John Yudkin. Tragically, their work, although supported by epidemiological evidence, became largely forgotten, Hujoel notes. This is unfortunate, he adds, because dental diseases really may be the most noticeable and rapid warning sign to an individual that something is going awry with his or her diet.

"Dental problems from poor dietary habits appear in a few weeks to a few years," Hujoel explains. "Dental improvement can be rapid when habits are corrected. For example, reducing sugar intake can often improve gingivitis scores (a measurement of gum disease) in a couple of weeks. Dental disease reveals very early on that eating habits are putting a person at risk for systemic disease. Because chronic medical disease takes decades to become severe enough to be detected in screening tests, dental diseases may provide plenty of lead-time to change harmful eating habits and thereby decrease the risk of developing the other diseases of civilization."

Ketone Bodies, Potential Therapeutic Uses

2009-10-14T14:36:00.000-05:00

Ketone Bodies, Potential Therapeutic Uses

Ketone Bodies, Potential Therapeutic Uses
Richard L. Veech, Britton Chance, Yoshihiro Kashiwaya, Henry A. Lardy, George F. Cahill Jr

Keywords
D-BETA-HYDROXYBUTYRATE • Ketone • Bodies • Ketosis • Metabolic • Control • Analysis • Neurologic • Disease

Abstract
Ketosis, meaning elevation of D- -hydroxybutyrate ( R -3-hydroxybutyrate) and acetoacetate, has been central to starving man's survival by providing nonglucose substrate to his evolutionarily hypertrophied brain, sparing muscle from destruction for glucose synthesis. Surprisingly, D- -hydroxybutyrate (abbreviated OHB) may also provide a more efficient source of energy for brain per unit oxygen, supported by the same phenomenon noted in the isolated working perfused rat heart and in sperm. It has also been shown to decrease cell death in two human neuronal cultures, one a model of Alzheimer's and the other of Parkinson's disease. These observations raise the possibility that a number of neurologic disorders, genetic and acquired, might benefit by ketosis. Other beneficial effects from OHB include an increased energy of ATP hydrolysis ( G') and its linked ionic gradients. This may be significant in drug-resistant epilepsy and in injury and anoxic states. The ability of OHB to oxidize co-enzyme Q and reduce NADP + may also be important in decreasing free radical damage. Clinical maneuvers for increasing blood levels of OHB to 2-5 mmol may require synthetic esters or polymers of OHB taken orally, probably 100 to 150 g or more daily. This necessitates advances in food-science technology to provide at least enough orally acceptable synthetic material for animal and possibly subsequent clinical testing. The other major need is to bring the technology for the analysis of multiple metabolic phenotypes up to the level of sophistication of the instrumentation used, for example, in gene science or in structural biology. This technical strategy will be critical to the characterization of polygenic disorders by enhancing the knowledge gained from gene analysis and from the subsequent steps and modifications of the protein products themselves.

Sept. 29, 1898: Stalin’s Scientist Sees First Light | This Day In Tech | Wired.com

2009-09-29T05:56:00.001-05:00

Sept. 29, 1898: Stalin’s Scientist Sees First Light | This Day In Tech | Wired.com

Early Soviet propagandists often relied on “miracles of science” to boost the status of their fledgling state. The young plant breeder Trofim Lysenko seemingly provided them with a whopper in 1927, reporting that he had developed a method of fertilizing fields without actually relying on fertilizers or minerals. The spinmeisters at Pravda had a field day, proclaiming that Lysenko had delivered on the Stalinist dream of using science to conquer nature.

Through a process he called “vernalization,” Lysenko reported growing peas in winter on the frozen steppe of Azerbaijan, causing Pravda to report breathlessly that Lysenko had turned …

the barren fields of the Trans-Caucasus green in winter, so that cattle will not perish from poor feeding, and the peasant Turk will live through the winter without trembling for tomorrow.

In fact, Lysenko’s methods were practically devoid of any science at all, and the “peasant Turk” continued to go hungry. But in a country where Joseph Stalin determined the truth and famine was ever present, the efficacy of vernalization was not to be denied. Top agricultural officials warmly embraced the process, and the tightly controlled state press dutifully pronounced it another miracle of Soviet science.

Except for the fact that crop vernalization didn’t work, it was, indeed, a miracle.

Lysenko’s star was definitely on the rise, thanks to officialdom’s alarming ability to ignore the facts in order to obtain the desired results. He also came to Moscow’s attention because of his talent for rallying the country’s peasantry, a surly segment of the population openly hostile to Stalinism. The hostility was thanks to Uncle Joe’s forced collectivization of small farms, which caused widespread starvation and the deaths of millions.

Lysenko, the semi-educated son of peasants, was able to put a human face on the regime back in the Kremlin. He spoke the peasants’ language and reassured them that science would fix everything.

He became a darling of Stalin’s, and after the dictator delivered a speech placing ideological needs above scientific research, Lysenko’s ascent was swift. In the early 1930s he was appointed head of the Academy of Agricultural Sciences and became the de facto arbiter of all the sciences, a mini-commissar, if you will. It was a catastrophe for Soviet science.

The little scientific theory absorbed by Lysenko came by way of Jean-Baptiste Lamarck, the early–19th-century French biologist who promulgated the theory, later refuted by Darwinism, that acquired characteristics could be passed from one generation to the next. This fit neatly with the Stalinist idea that nature could be manipulated to suit the needs of man.

Lysenko was hot-tempered, and he brooked no criticism of himself or his work. Legitimate Soviet geneticists and other scientists who dared oppose him often learned this hard truth with a one-way ticket to the gulag. Lysenko, in fact, despised his more-learned colleagues in a way that only a complete fraud with near-absolute power can.

He mercilessly rooted out perceived enemies of the state in what amounted to a crusade against science. With Stalin’s blessing, thousands of lab coats were shipped to Siberia, and hundreds died — or were killed — in the camps. In his own way, Lysenko proved to be as destructive to the Soviet Union as Stalin was with his purge of the Red Army officer corps.

For as long as Stalin lived, Lysenko was untouchable. After the dictator’s death in 1953, and his subsequent denunciation by Nikita Khrushchev at the 20th Communist Party Congress, Lysenko gradually lost influence. Although he held on to his offices for a time, scientists could now criticize him openly without fear of retribution. They did, with esteemed physicist Andrei Sakharov delivering the most withering blow in a 1964 address.

That same year, Lysenko saw his theories officially discredited and discarded by the Soviet Union. He was stripped of all his privileges, no small price to pay in Soviet society. In spite of everything, he kept showing up for work until his death in 1976.

Science thrown under the wagon in the name of politics. I think we're seeing similar things today, in terms of the "fat is bad for you" and "humans are warming the earth" theories. The government has already decided the answer to those two questions. Now do you want to help us save the world, or "confuse" people with contrary evidence?

Quest for a Long Life Gains Scientific Respect - NYTimes.com

2009-09-29T05:52:00.001-05:00

Quest for a Long Life Gains Scientific Respect - NYTimes.com

Some attendees were so convinced of the virtues of less food that they have begun severe diets of various kinds. Cynthia Kenyon, of the University of California, San Francisco, said she had gone on a low-carb diet in 2002 after finding that food with even 2 percent sugar reduced the lifespan of the laboratory roundworms she studies. “Basically I try to steer clear of desserts and starches, though I do eat chocolate,” she said.

Her willowy figure makes her look at least a decade younger than her age.

from wikipedia...

Personal diet

Kenyon's research prompted her to make personal dietary changes. She stopped eating high glycemic index carbohydrates when she discovered that putting sugar on the worms' food shortened their lifespans.[1]

Kenyon follows a low glycemic index diet similar to the Atkins diet[1] and the South Beach Diet[2].

No desserts. No sweets. No potatoes. No rice. No bread. No pasta. When I say ‘no,’ I mean ‘no, or not much,’ she notes. Instead, eat green vegetables. Eat the fruits that aren't the sweet fruits, like melon. Bananas? Bananas are a little sweet. Meat? Meat, yes, of course. Avocados. All vegetables. Nuts. Fish. Chicken. That's what I eat. Cheese. Eggs. And one glass of red wine a day.[3]

I have a fabulous blood profile. My triglyceride level is only 30, and anything below 200 is good.[3]

You have to eat something, and you just have to make your best judgement. And that's my best judgement. Plus, I feel better. Plus, I'm thin—I weigh what I weighed when I was in college. I feel great —you feel like you're a kid again. It's amazing.[3]

In the past, Kenyon had also briefly experimented with a calorie restriction diet for two days, but couldn't stand the constant hunger.[1]

Interesting. Over time, it seems as if the antioxidant theory of aging is losing ground to the insulin theory of aging. This scientist is applying her research to her own health.

Cardiovascular Diabetology | Full text | Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study

2009-09-25T17:16:00.000-05:00

Cardiovascular Diabetology | Full text | Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study

Results

Study participants had on average a diabetes duration of 9 years, a mean HbA1c of 6,6% units by Mono-S standard and were usually treated with metformin alone (3 subjects) or metformin in combination with a sulfonylurea (3 subjects) or a thiazolidinedione (3 subjects). Mean average dose of metformin was 1031 mg per day.

Compared to the diabetes diet, the Paleolithic diet resulted in lower mean values of
HbA1c (-0.4% units, p = 0.01),
triacylglycerol (-0.4 mmol/L, p = 0.003),
diastolic blood pressure (-4 mmHg, p = 0.03),
weight (-3 kg, p = 0.01), BMI (-1 kg/m2, p = 0.04) and waist circumference (-4 cm, p = 0.02), and
higher mean values of high density lipoprotein cholesterol (+0.08 mmol/L, p = 0.03).

The Paleolithic diet was mainly lower in cereals and dairy products, and higher in fruits, vegetables, meat and eggs, as compared with the Diabetes diet. Further, the Paleolithic diet was lower in total energy, energy density, carbohydrate, dietary glycemic load, saturated fatty acids and calcium, and higher in unsaturated fatty acids, dietary cholesterol and several vitamins. Dietary GI was slightly lower in the Paleolithic diet (GI = 50) than in the Diabetic diet (GI = 55).
Conclusion

Over a 3-month study period, a Paleolithic diet improved glycemic control and several cardiovascular risk factors compared to a Diabetes diet in patients with type 2 diabetes.

Men's Blood Pressure Increased By High-Sugar Diet

2009-09-25T17:13:00.000-05:00

Men's Blood Pressure Increased By High-Sugar Diet

Study 1 highlights:

* Just two weeks on a high-fructose diet raises blood pressure in men.

* A drug used to treat gout seems to protect against that blood pressure increase and some aspects of metabolic syndrome.

Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lower

2009-09-22T14:07:00.001-05:00

Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lowering statins -- Vishwanathan et al., 10.3945/ajcn.2009.28013 -- American Journal of Clinical Nutrition
ABSTRACT

Background: Lutein and zeaxanthin may reduce the risk of dry, age-related macular degeneration because of their photo-oxidative role as macular pigment.

Objective: The present study evaluated serum lutein, zeaxanthin, and macular pigment optical density (MPOD) responses at 0.25°, 0.5°, and 1° retinal eccentricities to the consumption of 2 and 4 egg yolks/d by older adults taking cholesterol-lowering medications.

Design: Subjects consumed foods containing 2 followed by 4 egg yolks/d for 5 wk each with a 4-wk egg-free period at baseline and between the 2 interventions.

Results: Changes in MPOD (n = 37) with egg yolk consumption were inversely associated (P < 0.05) with baseline MPOD. Subjects with low-baseline MPOD (defined as MPOD ≤0.5 at 0.25°, ≤0.4 at 0.5°, and ≤0.35 at 1°) showed increases of ≤50% (P < 0.05) with 4 egg yolks at the 3 retinal eccentricities. MPOD increased by 31% (P = 0.059) at 0.5° with 2 egg yolks. Serum lutein increased by only 16% and 24% (P < 0.05) compared with increases of 36% and 82% (P < 0.001) in serum zeaxanthin (n = 52) after consumption of 2 and 4 egg yolks, respectively. Serum HDL cholesterol increased by 5% (P < 0.05) after consumption of 2 and 4 egg yolks. Serum LDL cholesterol did not change with either egg yolk treatment.

Conclusions: Consumption of 4 egg yolks/d, and possibly of 2 egg yolks/d, for 5 wk benefited macular health in older adults with low MPOD. Serum HDL cholesterol increased without an increase in LDL cholesterol in this study population, most of whom were taking cholesterol-lowering statins.

low carb diet beats low fat for improving metabolic syndrome, again

2009-09-14T18:49:00.001-05:00

SpringerLink - Journal Article

Abstract We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (~1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (−12%) and insulin (−50%) concentrations, insulin sensitivity (−55%), weight loss (−10%), decreased adiposity (−14%), and more favorable triacylglycerol (TAG) (−51%), HDL-C (13%) and total cholesterol/HDL-C ratio (−14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (−47%), the Apo B/Apo A-1 ratio (−16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (−20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.

Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and High fructose corn syrup

2009-09-14T18:46:00.000-05:00

Obesity - Abstract of article: Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS-55

Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and insulin resistance. It is also a predisposing factor for type 2 diabetes. Dietary factors are believed to contribute to all three diseases. NAFLD is characterized by increased intrahepatic fat and mitochondrial dysfunction, and its etiology may be attributed to excessive fructose intake. Consumption of high fructose corn syrup-55 (HFCS-55) stands at up to 15% of the average total daily energy intake in the United States, and is linked to weight gain and obesity. The aim of this study was to establish whether HFCS-55 could contribute to the pathogenesis of NAFLD, by examining the effects of HFCS-55 on hepatocyte lipogenesis, insulin signaling, and cellular function, in vitro and in vivo. Exposure of hepatocytes to HFCS-55 caused a significant increase in hepatocellular triglyceride (TG) and lipogenic proteins. Basal production of reactive oxygen metabolite (ROM) was increased, together with a decreased capacity to respond to an oxidative challenge. HFCS-55 induced a downregulation of the insulin signaling pathway, as indicated by attenuated ser473phosphorylation of AKT1. The c-Jun amino-terminal kinase (JNK), which is intimately linked to insulin resistance, was also activated; and this was accompanied by an increase in endoplasmic reticulum (ER) stress and intracellular free calcium perturbation. Hepatocytes exposed to HFCS-55 exhibited mitochondrial dysfunction and released cytochrome C (CytC) into the cytosol. Hepatic steatosis and mitochondrial disruption was induced in vivo by a diet enriched with 20% HFCS 55; accompanied by hypoadiponectinemia and elevated fasting serum insulin and retinol-binding protein-4 (RBP4) levels.

Taken together our findings indicate a potential mechanism by which HFCS-55 may contribute to the pathogenesis of NAFLD.

ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome

2009-09-14T18:37:00.000-05:00

ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome

Background and aims

Carbohydrate restriction (CR) has been shown to improve dyslipidemias associated with metabolic syndrome (MetS). We evaluated the effects of CR on lipoprotein subfractions and apolipoproteins in Emirati adults classified with the MetS.
Methods and results

39 subjects (15 men/24 women) were randomly allocated to a CR diet [20–25% energy from carbohydrate (CHO)] for 12 wk (CRD group) or a combination treatment consisting of CRD for 6 wk followed by the American Heart Association diet (50–55% CHO, AHA group) for an additional 6 wk. All subjects reduced body weight, LDL cholesterol and triglycerides (P < 0.01). At baseline all subjects had low concentrations of medium VLDL and total HDL particles associated with the very low plasma triglycerides and HDL cholesterol in this population. After 12 wk, the large VLDL subfraction was decreased over time for subjects in the CRD group (P < 0.01) while these changes were not observed in those subjects who changed to the AHA diet. The number of medium and small LDL particles decreased for all subjects rendering a less atherogenic lipoprotein profile. In agreement with these results, a significant decrease in apolipoprotein (apo) B was observed (P < 0.01). The medium HDL subfraction and apo A-II, which can be considered pro-atherogenic, were also decreased over time in the CRD group only.

Conclusions

These results suggest that weight loss favorably affects lipoprotein metabolism and that the CRD had a better effect on atherogenic VLDL and HDL than the low fat diet recommended by AHA.

High protein intake reduces intrahepatocellular lipid deposition in humans -- Bortolotti et al., 10.3945/ajcn.2008.27296 -- American Journal of Clinical Nutrition

2009-09-07T21:36:00.000-05:00

High protein intake reduces intrahepatocellular lipid deposition in humans -- Bortolotti et al., 10.3945/ajcn.2008.27296 -- American Journal of Clinical Nutrition

Background: High sugar and fat intakes are known to increase intrahepatocellular lipids (IHCLs) and to cause insulin resistance. High protein intake may facilitate weight loss and improve glucose homeostasis in insulin-resistant patients, but its effects on IHCLs remain unknown.

Objective: The aim was to assess the effect of high protein intake on high-fat diet–induced IHCL accumulation and insulin sensitivity in healthy young men.

Increasing protein in the diet reduces the dangerous buildup of fat in the liver. This fatty liver problem is fond in alcoholics and people consuming large amounts of fructose, i.e. metabolic syndrome.

Access : Connecting obesity, aging and diabetes : Nature

2009-09-07T16:38:00.001-05:00

Access : Connecting obesity, aging and diabetes : Nature:

"Obesity accelerates the aging of adipose tissue, a process only now beginning to come to light at the molecular level. Experiments in mice suggest that obesity increases the formation of reactive oxygen species in fat cells, shortens telomeres—and ultimately results in activation of the p53 tumor suppressor, inflammation and the promotion of insulin resistance (pages 1082–1087).

Obesity accelerates the aging of adipose tissue, leading to inflammation and insulin resistance.

As technology has improved hygiene, the food supply and living standards overall, there has been a rise in such age-related illnesses as cardiovascular disease, cancer, degenerative diseases of the brain and other organs, and metabolic disorders such as diabetes. Age-related disorders have become widespread throughout the world, replacing infectious diseases as the leading cause of death in developed countries."

Over 70% of American children deficient in vitamin D! - Kumar et al. 124 (3): e362 -- Pediatrics

2009-09-07T16:37:00.000-05:00

Prevalence and Associations of 25-Hydroxyvitamin D Deficiency in US Children: NHANES 2001-2004 -- Kumar et al. 124 (3): e362 -- Pediatrics:

OBJECTIVES: To determine the prevalence of 25-hydroxyvitamin D (25[OH]D) deficiency and associations between 25(OH)D deficiency and cardiovascular risk factors in children and adolescents.

"CONCLUSIONS: 25(OH)D deficiency is common in the general US pediatric population and is associated with adverse cardiovascular risks."

Over 70% of American children deficient in vitamin D!