Friday, September 28, 2007

Excerpt: 'Good Calories, Bad Calories'

Excerpt: 'Good Calories, Bad Calories'

Read an Excerpt: 'Good Calories, Bad Calories'
Author Challenges What We Thought We Knew About Nutrition

Sept. 27, 2007 —

What if everything you think you know about diet and exercise, even disease, turned out to be wrong?

A new book called "Good Calories, Bad Calories" suggests just that. And it's causing a storm of controversy-- think saturated fats are bad for you? Think again. Think exercise will slim you down? Not true. At least that's what Gary Taubes thinks -- he says he's reviewed the research and interviewed over 600 experts and has the evidence to prove it.

Read an excerpt from his book, "Good Calories, Bad Calories," below.

Good Calories, Bad Calories

I have spent much of the last fifteen years reporting and writing about issues of public health, nutrition, and diet. I have spent five years on the research for and writing of this book alone. To a great extent, the conclusions I've reached are as much a product of the age we live in as they are my own skeptical inquiry. Just ten years ago, the research for this book would have taken the better part of a lifetime. It was only with the development of the Internet, of search engines and the comprehensive databases of the Library of Medicine, the Institute for Scientific Information, research libraries, and secondhand-book stores worldwide now accessible online that I was able, with reasonable facility, to locate and procure virtually any written source, whether published a century ago or last week, and to track down and contact clinical investigators and public-health officials, even those long retired.

Throughout this research, I tried to follow the facts wherever they led. In writing the book, I have tried to let the science and the evidence speak for themselves. When I began my research, I had no idea that I would come to believe that obesity is not caused by eating too much, or that exercise is not a means of prevention. Nor did I believe that diseases such as cancer and Alzheimer's could possibly be caused by the consumption of refined carbohydrates and sugars. I had no idea that I would find the quality of the research on nutrition, obesity, and chronic disease to be so inadequate; that so much of the conventional wisdom would be founded on so little substantial evidence; and that, once it was, the researchers and the public-health authorities who funded the research would no longer see any reason to challenge this conventional wisdom and so to test its validity.

As I emerge from this research, though, certain conclusions seem inescapable to me, based on the existing knowledge:

1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.

2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasisthe entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.

3. Sugarssucrose and high-fructose corn syrup specificallyare particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.

4. Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer's disease, and the other chronic diseases of civilization.

5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

7. Fattening and obesity are caused by an imbalancea disequilibriumin the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.

8. Insulin is the primary regulator of fat storage. When insulin levels are elevatedeither chronically or after a mealwe accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.

9. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.

10. By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.

In considering these conclusions, one must address the obvious question: can a diet mostly or entirely lacking in carbohydrates possibly be a healthy pattern of eating? For the past half century, our conceptions of the interaction between diet and chronic disease have inevitably focused on the fat content. Any deviation from some ideal low-fat or low-saturated-fat diet has been considered dangerous until long-term, randomized control trials might demonstrate otherwise. Because a diet restricted in carbohydrates is by definition relatively fat-rich, it has therefore been presumed to be unhealthy until proved otherwise. This is why the American Diabetes Association even recommends against the use of carbohydrate-restricted diets for the management of Type 2 diabetes. How do we know they're safe for long-term consumption?

The argument in their defense is the same one that Peter Cleave made forty years ago, when he proposed what he called the saccharine-disease hypothesis. Evolution should be our best guide for what constitutes a healthy diet. It takes time for a population or a species to adapt to any new factor in its environment; the longer we've been eating a particular food as a species, and the closer that food is to its natural state, the less harm it is likely to do. This is an underlying assumption of all public-health recommendations about the nature of a healthy diet. It's what the British epidemiologist Geoffrey Rose meant when he wrote his seminal 1985 essay, "Sick Individuals and Sick Populations," and described the acceptable measures of prevention that could be recommended to the public as those that remove "unnatural factors" and restore " 'biological normality'that is . . . the conditions to which presumably we are genetically adapted." "Such normalizing measures," Rose said, "may be presumed to be safe, and therefore we should be prepared to advocate them on the basis of a reasonable presumption of benefit."

The fat content of the diets to which we presumably evolved, however, will always remain questionable. If nothing else, whatever constituted the typical Paleolithic hunter-gatherer diet, the type and quantity of fat consumed assuredly changed with season, latitude, and the coming and going of ice ages. This is the problem with recommending that we consume oils in any quantity. Did we evolve to eat olive oil, for example, or linseed oil? And maybe a few thousand years is sufficient time to adapt to a new food but a few hundred is not. If so, then olive oil could conceivably be harmless or even beneficial when consumed in comparatively large quantities by the descendants of Mediterranean populations, who have been consuming it for millennia, but not to Scandinavians or Asians, for whom such an oil is new to the diet. This makes the science even more complicated than it already is, but these are serious considerations that should be taken into account when discussing a healthy diet.

There is no such ambiguity, however, on the subject of carbohydrates. The most dramatic alterations in human diets in the past two million years, unequivocally, are (1) the transition from carbohydrate-poor to carbohydrate-rich diets that came with the invention of agriculturethe addition of grains and easily digestible starches to the diets of hunterepilogue gatherers; (2) the increasing refinement of those carbohydrates over the past few hundred years; and (3) the dramatic increases in fructose consumption that came as the per-capita consumption of sugarssucrose and now high-fructose corn syrupincreased from less than ten or twenty pounds a year in the mid-eighteenth century to the nearly 150 pounds it is today. Why would a diet that excludes these foods specifically be expected to do anything other than return us to "biological normality"?

It is not the case, despite public-health recommendations to the contrary, that carbohydrates are required in a healthy human diet. Most nutritionists still insist that a diet requires 120 to 130 grams of carbohydrates, because this is the amount of glucose that the brain and central nervous system will metabolize when the diet is carbohydrate-rich. But what the brain uses and what it requires are two different things. Without carbohydrates in the diet, as we discussed earlier (see page 319), the brain and central nervous system will run on ketone bodies, converted from dietary fat and from the fatty acids released by the adipose tissue; on glycerol, also released from the fat tissue with the breakdown of triglycerides into free fatty acids; and on glucose, converted from the protein in the diet. Since a carbohydrate-restricted diet, unrestricted in calories, will, by definition, include considerable fat and protein, there will be no shortage of fuel for the brain. Indeed, this is likely to be the fuel mixture that our brains evolved to use, and our brains seem to run more efficiently on this fuel mixture than they do on glucose alone. (A good discussion of the rationale for a minimal amount of carbohydrates in the diet can be found in the 2002 Institute of Medicine [IOM] report, Dietary Reference Intakes. The IOM sets an "estimated average requirement" of a hundred grams of carbohydrates a day for adults, so that the brain can run exclusively on glucose, "without having to rely on a partial replacement of glucose by [ketone bodies]." It then sets the "recommended dietary allowance" at 130 grams to allow margin for error. But the IOM report also acknowledges that the brain will be fine without these carbohydrates, because it runs perfectly well on ketone bodies, glycerol, and the protein-derived glucose.)

Whether a carbohydrate-restricted diet is deficient in essential vitamins and minerals is another issue. As we also discussed (see page 32026), animal products contain all the amino acids, minerals, and vitamins essential for health, with the only point of controversy being vitamin C. And the evidence suggests that the vitamin C content of meat products is more than sufficient for health, as long as the diet is indeed carbohydraterestricted, with none of the refined and easily digestible carbohydrates and sugars that would raise blood sugar and insulin levels and so increase our need to obtain vitamin C from the diet. Moreover, though it may indeed be uniquely beneficial to live on meat and only meat, as Vilhjalmur Stefannson argued in the 1920s, carbohydrate-restricted diets, as they have been prescribed ever since, do not restrict leafy green vegetables (what nutritionists in the first half of the twentieth century called 5 percent vegetables) but only starchy vegetables (e.g., potatoes), refined grains and sugars, and thus only those foods that are virtually without any essential nutrients unless they're added back in the processing and so fortified, as is the case with white bread. A calorie-restricted diet that cuts all calories by a third, as John Yudkin noted, will also cut essential nutrients by a third. A diet that prohibits sugar, flour, potatoes, and beer, but allows eating to satiety meat, cheese, eggs, and green vegetables will still include the essential nutrients, whether or not it leads to a decrease in calories consumed.

Gary Taubes' new book comes out soon!

New findings support theory on Alzheimer's as a form of diabetes - Science News - QJ.NET

New findings support theory on Alzheimer's as a form of diabetes - Science News - QJ.NET

New findings have revealed that the memory-losing disease, Alzheimer's, is actually a form of diabetes. Northwestern University scientists have discovered that the toxic protein "amyloid ß-derived diffusible ligand" - or ADDL - takes away the insulin receptors from the nerve cells, thereby making them insulin resistant.

Hampering insulin and its receptors to the brain results to memory loss as the two are key components in memory formation. Now having determined that Alzheimer's may be caused in part by this insulin resistance, thanks to the attack of ADDL, the next question to confront then would be how this attack is triggered.

Weinberg College's William L. Klein, leader of the research, explains:

We think this is a major factor in the memory deficiencies caused by ADDLs in Alzheimer's brains. We're dealing with a fundamental new connection between two fields, diabetes and Alzheimer's disease, and the implication is for therapeutics. We want to find ways to make those insulin receptors themselves resistant to the impact of ADDLs. And that might not be so difficult.

The Role of Insulin in Human Brain Glucose Metabolism: An 18Fluoro-Deoxyglucose Positron Emission Tomography Study -- Bingham et al. 51 (12): 3384 -- Diabetes

The Role of Insulin in Human Brain Glucose Metabolism: An 18Fluoro-Deoxyglucose Positron Emission Tomography Study -- Bingham et al. 51 (12): 3384 -- Diabetes

Our study results challenge the accepted view that human brain glucose uptake is an entirely insulin-independent process. Instead, our data suggest that there is a significant element of brain glucose uptake that is insulin sensitive, with a dose-response curve that is shifted well to the left of dose-response curves for other insulin-sensitive tissues, such as muscle or liver. Previous studies have demonstrated no change in rate of brain glucose metabolism in response to elevations of circulating insulin above the basal (fasting) range (19,22). Our data, examining the effect of basal insulin replacement during somatostatin infusion, show that brain glucose uptake is however partially insulin sensitive, as there was a significant reduction in global brain glucose uptake when circulating insulin levels were reduced below this. Coupled with the published data showing no effect of increasing circulating insulin above fasting levels, we can infer that brain glucose metabolism is maximally stimulated at these fasting insulin concentrations. The magnitude of the effect may not seem large, but this is because it is superimposed on a background of insulin-independent brain glucose uptake. A 15% increase in brain glucose uptake secondary to insulin stimulation may have clinical significance.

It would follow then that insulin insensitivity caused by lots of carbs would block the flow of glucose to your brain as well as your body.

Thursday, September 27, 2007

Not Just DRD2: Gene That May Influence Alcoholism And Addiction Identified

ScienceDaily: Gene That May Influence Alcoholism And Addiction Identified

Riley explained that genetic research can often be guided by additional non-genetic information. "We know that certain regions of the brain are particularly important in processing reward," he said. "Neurons which use dopamine as their neurotransmitter connect these regions, and some research suggests that there may be dopamine imbalances in these regions among alcoholics. Although these differences might be the result of chronic heavy drinking rather than its cause ... variation in genes coding for the various proteins that mediate dopamine neurotransmission might also be involved in alcoholism. The DRD2 gene, which codes for one of the five dopamine receptors, has been heavily studied for possible links to alcoholism, but with mixed results. Hence the current study."

Using data collected as part of the Collaborative Study on the Genetics of Alcoholism (COGA), a long-term project with multiple sites across the United States, researchers genotyped 26 single-nucleotide polymorphisms (SNPs) spanning DRD2 and ANKK1 in a sample of 219 Caucasian families (n=1923).

"The key finding here is that when you genotype markers not just in DRD2, the highly studied gene in this region, but also genotype markers across surrounding genes, there is evidence that surrounding genes, such as ANKK1, may also be involved in addiction phenotypes," said Dick. "If there are indeed multiple genes in the region involved, it may help explain the inconsistency surrounding whether DRD2 plays a role."

Riley concurs. "The study finds strongest evidence of association not in the DRD2 gene, but rather in the neighboring gene, ANKK1," he said. "This is notable because it suggests that the original evidence pointed to ANKK1 all along and it was the error in mapping the variant that supported the involvement of DRD2. However, the evidence in this paper is by no means conclusive that ANKK1 is involved in alcoholism, any more than the older evidence was that DRD2 was involved, and it must be interpreted with caution and further explored."

Thursday, September 20, 2007

Fighting Cancer with Low Carb

Jimmy Moore's Livin' La Vida Low-Carb™ Blog

In the article entitled "Can A High-Fat Diet Beat Cancer?" (although I'm not sure what that big double cheeseburger at the top of this story has ANYTHING at all to do with a high-fat, low-carb diet--that bad boy is MUCH higher in carbs from that big ole bun!), researchers Dr. Melanie Schmidt and Ulrike Kammerer, both from the University of Wurzburg in Germany, have been implementing the use of a high-fat, low-carb ketogenic diet on the most dire of cancer patients who have run out of treatment options since the beginning of the year. Without the use of any medications, they simply require the participants to slash their carbs and eat more fat.

By getting rid of virtually all the carbs in their diet, especially sugar which feeds cancer cells, the researchers replace that energy with healthy fat sources including hempseed and linseed oils, soy-based proteins, and animal fats and proteins. It's a supercharged version of the Atkins diet and more closely resembles the original low-carb diet plan from the late great Dr. Robert C. Atkins released back in 1972.

Ketones help ADD symptoms

Food and Behaviour Research: Murphy & Burnham 2006 - The ketogenic diet causes a reversible decrease in activity level in Long-Evans rats

The ketogenic diet causes a reversible decrease in activity level in Long-Evans rats
Murphy P, Burnham WM. (2006) Exp Neurol. 201(1) 84-9. Epub 2006 Jun 5
Web URL: View this and related abstracts via Pubmed here

Abstract: Individuals with epilepsy also often exhibit symptoms of attention deficit hyperactivity disorder (ADHD). The ketogenic diet, which is a high fat, low protein, and low carbohydrate diet used in the treatment of intractable epilepsy, also appears to improve symptoms of ADHD in individuals with both disorders. Previous research suggests that the diet decreases the activity level of rats. The purpose of the present research was to further investigate the effects of the ketogenic diet on activity level, using an animal model. Two experiments were conducted. The first experiment examined the time frame and reversibility of the effect of the diet on activity level. The second experiment examined the relationship between activity level and anxiety level. In both experiments, adult male Long-Evans rats were placed on either a ketogenic diet or a control diet. The results of the first experiment show that the ketogenic diet can cause a decrease in activity level within 24 h and that the results are reversible. The results of Experiment 2 show that the decrease in activity level is not linked to a change in anxiety level. The ketogenic diet may be of use in the treatment of ADHD.

FAB Research Comment:

While it's too early to draw conclusions from this study to the management of ADHD in humans, it's of obvious interest that activity levels were reversibly lowered with this dietary intervention. The same diet has previously been found to ameliorate some aspects of mood disorder in animal models (see Murphy et al 2004).

It is unfortunate that many reports refer to so-called 'high-fat' diets without emphasising that different *types* of fat have very different implications for both physical health and brain function. A very low intake of protein and carbohydrate can also have serious side-effects.

The ketogenic diet is already used in some cases for the management of serious epilepsy, but in our view, no such diet as this should ever be attempted without expert professional advice. For more practical dietary information on the management of ADHD

Alzheimer's May Be Tied To High Blood Sugar -

Alzheimer's May Be Tied To High Blood Sugar -

People with elevated blood sugar levels may have an increased risk of developing Alzheimer's disease, researchers reported yesterday at an international conference.

Scientists already have linked Type 2 diabetes with Alzheimer's, which afflicts 4.5 million Americans.

But researchers from Stockholm's Karolinska Institute said the link to Alzheimer's disease may take hold earlier, in people who have higher-than-normal blood sugar levels but not in the diabetic range -- a condition known as pre-diabetes.

Pre-diabetes affects 41 million Americans between the ages of 40 and 74, according to the American Diabetes Association, while diabetes has been diagnosed in 14.6 million Americans.

The Karolinska researchers presented their nine-year study of more than 1,100 people on the opening day of the 10th International Conference on Alzheimer's Disease and Related Disorders in Madrid.

Alzheimer's disease robs the brain of its memory and processing skills. The number of victims is expected to grow fourfold by the middle of the century as the population ages and baby boomers reach retirement, according to the Chicago-based Alzheimer's Association.

Wednesday, September 19, 2007

McCleary: Ketone Bodies Produced By A Low-Carb Diet Are High-Octane Brain Food

Jimmy Moore's Livin' La Vida Low-Carb™ Blog: McCleary: Ketone Bodies Produced By A Low-Carb Diet Are High-Octane Brain Food

McCleary: Ketone Bodies Produced By A Low-Carb Diet Are High-Octane Brain Food
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Dr. Larry McCleary says sharpen your brain by livin' la vida low-carb

It doesn't take a brain surgeon to figure out that the low-carb lifestyle is one of the healthiest nutritional plans out there to battle obesity, heart disease, diabetes, and so many other health ailments that plague modern society. But what about that actual gray matter between our ears? Can a low-carb diet do anything to improve brain function, memory, and even diseases like Alzheimer's?

One of America's top neurosurgeons says YES!

His name is Dr. Larry McCleary and his brand new book about this subject entitled The Brain Trust Program: A Scientifically Based Three-Part Plan to Improve Memory, Elevate Mood, Enhance Attention, Alleviate Migraine and Menopausal Symptoms, and Boost Mental Energy released today. I'm happy to share an exclusive interview I conducted with Dr. McCleary with you today so we can all learn from one of the brightest minds in the field of cognitive health.


Brain health entails more than most people even realize as you so brilliantly share in your brand new book entitled The Brain Trust Program. It is an outstanding resource that I was privileged to review and in it you share a three-part method for actually improving brain function through the use of diet, supplementation, and brain exercises. How does your novel new approach differ from the most common ways to correct brain abnormalities and conditions?

Jimmy, I think we have all heard that the brain burns glucose, or sugar. So if that's the case, then giving it lots of sugar must make it work better. Although that might seem logical, the science doesn't back it up. Just the opposite, there is a groundswell of medical evidence that documents how too much sugar can make the brain shrink, wither, atrophy and just plain work badly.

If you want to age your brain just eat the typical diet most Americans consume. That will lead to memory, attention and mood difficulties and will hasten the path to Alzheimer's. The Brain Trust Program builds upon this concept and provides the science behind the recommendations.

3. Many eyebrows will certainly be raised when people find out what a “brain-healthy diet” actually looks like. Foods like fish, berries, green leafy vegetables, eggs, avocados, nuts, seeds, and coffee—conspicuously all low-sugar and low-carb, by the way—are highly recommended by you for maximized brain function. It falls right in line with the latest research for neurological diseases.

Essentially, you are stating that the health of the brain is directly tied to blood sugar levels in the body—something that medical literature confirms. I’m sure some of your colleagues will no doubt scoff at your contention that a simple nutritional approach is what is needed to preserve this most vital of our organs.

What led you to go down this path for treating your patients? Have you seen similar or better improvements in brain health compared with prescription drugs and other treatment options?

As you well know, prescription drugs usually act on a single metabolic, or cellular, pathway. By increasing or decreasing a specific functions, drugs might be able to treat something like an under-active thyroid. However, all of the diseases associated with aging such as heart disease, arthritis, thinning of bones, memory loss and stroke are hardly changed by drug therapy. The key question is why.

As we have seen, drugs act on a single highly specialized pathway. The diseases that cause most concern today involve disruption to multiple cellular pathways. That is why the pharmaceutical industry has failed us. We need a solution that improves MANY cellular functions. This is the very act of eating well. It is also closely tied to our DNA and evolutionary history. Simply stated, that is why nutrition is so important and so beneficial.


Diabetes has become the health crisis of our time with millions of new cases popping up every year while its twin epidemic obesity continues to get worse and worse. We all know about Type 1 and Type 2 diabetes, but what about this new version some researchers are calling “Type 3 diabetes” which is the new way of referring to Alzheimer’s Disease because of the impact sugar has on this condition?

I've highlighted several published studies here at my blog showing various versions of a low-carb diet can effectively reverse the symptoms of this condition, including one study by Dr. Thomas Seyfried from Boston College in February 2007 using a high-fat, low-carb diet to actually shrink brain cancer tumors. What has been your experience with treating brain diseases like these through innovative dietary improvements compared with the recommended Standard American Diet?

Type 3 diabetes as you have referred to, was a phrase coined by researchers at Brown University. It suggests that the brain is unable to effectively use glucose as a fuel, much the same as the body of a diabetic can no longer use glucose as a fuel. The ability to deliver a low, stable and continuous supply of glucose to the brain is what makes it most happy.

The dramatic spikes, surges, or continuous excessive supply delivered by today's diet is toxic for the brain. It is now well-known that insulin resistance, glucose intolerance, or the worst form of sugar problem--diabetes, ages the brain and doubles the risk for all types of memory problems and even Alzheimers disease. As you have suggested, the types of fats and carbohydrates in our diets are key in accomplishing this goal.

We need to include more of the brain-friendly omega 3 fats and veggies and fruits (especially berries), and less of the refined carbohydrates such as cakes, cookies, and breads and trans fats in items like margarine.

8. Many of my readers who deal with less severe brain conditions like migraine headaches, menopause, hot flashes, dimming of the senses, brain fog, and memory loss will be pleased to learn that you actually recommend a specific “cocktail” for each of these in your book. Fascinating! Each of these contains all-natural and healthy ingredients that will supercharge your brain and make it better and stronger than ever.

Give us an example of your most prescribed “cocktail” for a common brain ailment. How quickly can people expect to find relief for their condition using these treatment options and will they need to keep up these regimens for the rest of their lives?

Many common conditions of the brain are directly related to its inability to produce the energy it needs to get through the day. Our brains are being asked to do more today than ever before. They consume energy 10x faster than the rest of the body. Our dietary and lifestyle choices impair the brain's ability to meet these energy needs which depend upon glucose.

The suggestions I make in The Brain Trust Program depend on an alternative energy source the body developed millions of years ago for times when the brain couldn't depend upon glucose. This alternative fuel is ketone bodies which are merely partially burned fats. They are burned differently than sugars and the brain loves them.

They have been shown to help a multitude of brain afflictions from memory loss to migraine headaches to hot flashes. They are generated in the body from a nutritional supplement called pure MCT (medium chain triglyceride) oil that is available from high end vitamin stores or on the internet. When consumed the results and response can be surprising and may be measured in days! Another easy way to produce ketone bodies is simply by restricting carbohydrate intake.

9. You are a big believer in the body’s use of the ketone bodies that form in a carb-restricted state for optimal brain health. What has your research on ketones shown you to make you so confident that they are an excellent replacement for glucose as fuel for the brain? What is your professional response to those who oppose a low-carb nutritional approach as an unhealthy, dangerous, fad diet that is potentially harmful and deadly over the long-term?

Fad diets come and go. The diet we cut our evolutionary teeth on is essentially a low-carb diet that generates high levels of ketone bodies. You need look no further than the brains of children with intractable seizures to see how miraculous ketones are for brain health and function. They work where all drugs fail by increasing the energy available for the nerve cells and keeping them from becoming over-excited which is after all what causes seizures to develop in the first place.

Blog: High Blood Sugar Likely Induces Alzheimer's

Jimmy Moore's Livin' La Vida Low-Carb™ Blog: High Blood Sugar Likely Induces Alzheimer's

New research highlights the role sugar plays in Alzheimer's disease

This Washington Post column about a newfound connection between blood sugar and the onset of Alzheimer's disease should give give the 73 million Americans currently diagnosed with diabetes or pre-diabetes reason enough to start livin' la vida low-carb to prevent this from happening to them.

Researchers from the Stockholm, Sweden-based Karolinska Institute presented their 9-year study of over 1,100 people at the 10th International Conference on Alzheimer's Disease and Related Disorders in Madrid, Spain on Monday.

What they found during their research is that people with high blood sugar levels are at a higher risk of developing Alzheimer's disease. Previous studies have already shown a link between Type 2 diabetes and Alzheimer's, but this new research now reveals that even pre-diabetics who have not developed full-blown diabetes yet are in danger of getting the brain-altering Alzheimer's disease.

The Alzheimer's Association has already predicted the number of cases of Alzheimer's disease is expected to quadruple by the year 2050 as the progression of this disease correlates directly with the diabetes epidemic that is now underway.

I have previously blogged about why diabetes can't be cured yet and now we see the unintended consequences of our inability to consider all the treatment options for type 2 diabetes. With the most recent research pointing to the low-carb approach as the best way to help diabetics control their blood sugar levels without the use of medications, then why wouldn't we want to use this miraculous way of eating to slow down the rates of Alzheimer's disease as well?

In fact, we've already seen another recent study that showed a low-carb diet can actually REVERSE Alzheimer's disease completely which went hand-in-hand with this study showing a high-fat, nearly zero-carb diet controlled the symptoms of yet another debilitating neurological disease -- Parkinson's!

The evidence is clear to anyone who is paying attention and can still comprehend what is going on here. Diseases of the brain such as Alzheimer's and Parkinson's are very likely caused by the excessive amounts of sugar we are putting in our mouths which is then leading to the twin health epidemics of obesity and diabetes that brings us back to a higher risk for developing these awful diseases. Eeeek!

Study: High-Carb, Low-Fat Or Low-Carb, High Fat Diet Equally Lower Weight, Improve Mood And Memory

Study: High-Carb, Low-Fat Or Low-Carb, High Fat Diet Equally Lower Weight, Improve Mood And Memory

Think a low-carb diet will destroy your brain? Think again!

It was a head-to-head match-up that ended in a tie.

Just wait until you see the stunning results of a new study comparing the traditional high-carb, low-fat diet with the increasingly popular low-carb, high-fat diet as it relates not just to weight loss, but also brain function. Now this oughta be interesting!

I recently interviewed one of the premier neurologists in the world named Dr. Larry McCleary who promotes carbohydrate-restriction as a means for improving brain health in his recently released book entitled The Brain Trust Program. He said something in that interview that should make anyone who advocates a high-carb diet for brain health to stop and think.

"If you want to age your brain just eat the typical [high-carb] diet most Americans consume. That will lead to memory, attention and mood difficulties and will hasten the path to Alzheimer's."

Yikes! That's pretty scary if you ask me and it goes against everything we've always been led to believe about diet and the way our brain reacts. Of course, the popular stereotype of someone who is livin' la vida low-carb is that you just walk around in a perpetual sense of depression and rage all the time like you're some kind of zombie or something!

In fact, there's even a YouTube video that attempts to illustrate and perpetuate this myth about low-carb diets claiming people who eat this way are "damaging their brains." Yeah, whatever!

But according to the study conducted by lead researcher Angela K. Halyburton, from the Commonwealth Scientific and Industrial Research Organization (CSIRO) in the Department of Human Nutrition in Adelaide, Australia, that myth is just that--an unproven and unreasonable conclusion that is not based on the evidence. That's because what she and her colleagues found was a surprising answer to the questions about diet and mood.

Halyburton and her fellow researchers observed 93 overweight or obese study participants who were placed on one of two specific diets with an appropriate fat/protein/carbohydrate ratio:

LCHF--an Atkins-like low-carb, high-fat diet--61/35/4
(NOTE: 20 percent of the fat intake was saturated)


HCLF--a traditional high-carb, low-fat diet--30/24/46

Both groups were given the same number of calories and consumed their respective diets for a total of eight weeks on this randomized, clinical trial. Study participants were weighed every two weeks and given a psychological well-being test based on the Profile of Mood States, Beck Depression Inventory, and Spielberger State Anxiety Inventory instruments. The researchers measured cognitive function, memory, and speed of brain processing at the beginning and end of the study.

Not surprisingly, the LCHF group participants were already in ketosis by the end of the first two weeks of carbohydrate-restriction and remained there for the duration of the study. As a result, they lost "significantly" more weight than their HCLF diet counterparts. Gee, imagine that!

But the real surprise was the fact that improvements in the mood of the participants in BOTH groups improved. That's right! Despite all the stereotypes about low-carb, the psychological improvements in attitude and memory function were IDENTICAL with both the high-carb, low-fat diet group and the low-carb, high-fat diet group. It didn't matter. WOW!!! This is HUGE!

The only area where there was a difference regarding brain function was with the speed of processing information. According to the study, the LCHF group responded slower than the HCLF diet group. But the overall conclusion of the researchers was that these two diets which have often been compared for weight loss alone also show no difference as it relates to cognitive and psychological function.

Can a High-Fat Diet Beat Cancer? - TIME

Can a High-Fat Diet Beat Cancer? - TIME
Since early 2007, Dr. Melanie Schmidt and biologist Ulrike Kammerer, both at the Wurzburg hospital, have been enrolling cancer patients in a Phase I clinical study of a most unexpected medication: fat. Their trial puts patients on a so-called ketogenic diet, which eliminates almost all carbohydrates, including sugar, and provides energy only from high-quality plant oils, such as hempseed and linseed oil, and protein from soy and animal products.

What sounds like yet another version of the Atkins craze is actually based on scientific evidence that dates back nearly 80 years. In 1924, the German Nobel laureate Otto Warburg first published his observations of a common feature he saw in fast-growing tumors: unlike healthy cells, which generate energy by metabolizing sugar in their mitochondria, cancer cells appeared to fuel themselves exclusively through glycolysis, a less-efficient means of creating energy through the fermentation of sugar in the cytoplasm. Warburg believed that this metabolic switch was the primary cause of cancer, a theory that he strove, unsuccessfully, to establish until his death in 1970.

To the two researchers in Wurzburg, the theoretical debate about what is now known as the Warburg effect — whether it is the primary cause of cancer or a mere metabolic side effect — is irrelevant. What they believe is that it can be therapeutically exploited. 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 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," Kammerer 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. So far, it's impossible to predict whether it will really work. It is already evident that it doesn't always: two patients recently left the study because their tumors kept growing, even though they stuck to the diet.

Past studies, however, offer some hope. The first human experiments with the ketogenic diet were conducted in two children with brain cancer by Case Western Reserve oncologist Linda Nebeling, now with the National Cancer Institute. Both children responded well to the high-fat diet. When Nebeling last got in contact with the patients' parents in 2005, a decade after her study, one of the subjects was still alive and still on a high-fat diet. It would be scientifically unsound to draw general conclusions from her study, says Nebeling, but some experts, such as Boston College's Thomas Seyfried, say it's still a remarkable achievement. Seyfried has long called for clinical trials of low-carb, high-fat diets against cancer, and has been trying to push research in the field with animal studies: His results suggest that mice survive cancers, including brain cancer, much longer when put on high-fat diets, even longer when the diets are also calorie-restricted. "Clinical studies are highly warranted," he says, attributing the lack of human studies to the medical establishment, which he feels is single-minded in its approach to treatment, and opposition from the pharmaceutical industry, which doesn't stand to profit much from a dietetic treatment for cancer.

The tide appears to be shifting. A study similar to the trial in Wurzburg is now under way in Amsterdam, and another, slated to begin in mid-October, is currently awaiting final approval by the ethics committee at the University Hospital in Tubingen, Germany. There, in the renowned old research institution in the German southwest, neuro-oncologist Dr. Johannes Rieger wants to enroll patients with glioblastoma and astrocytoma, aggressive brain cancers for which there are hardly any sustainable therapies. Cell culture and animal experiments suggest that these tumors should respond particularly well to low-carb, high-fat diets. And, usually, these patients are physically sound, since the cancer affects only the brain. "We hope, and we have reason to believe, that it will work," says Rieger.

Still, none of the researchers currently studying ketogenic diets, including Rieger, expects it to deliver anything close to a universal treatment for cancer. And none of them wants to create exaggerated hopes for a miracle cure in seriously ill patients, who may never benefit from the approach. But the recent findings are difficult to ignore. Robert Weinberg, a biology professor at MIT's Whitehead Institute who discovered the first human oncogene, has long been critical of therapeutic approaches based on the Warburg effect, and has certainly dismissed it as a primary cause of cancer. Nevertheless, he conceded, in an email, for tumors that have been affected by the ketogenic diet in animal models, "there might be some reason to go ahead with a Phase I clinical trial, especially for patients who have no other realistic therapeutic options."

This article is about the warburg effect, which refers to a property of cancer cells in which they use primarily who grows as a fuel. Some believe that limiting carbohydrates in the diet could starve cancer cells. The cancer cells would die while normal body and brain cells should be able to handle the sugar starvation they can generate energy from ketones instead.

It is interesting that they had to work with the worst cancer patients, yet even so many of the patients found it difficult to completely renounce soft drinks chocolates and other high carbohydrate foods, even though they improved on the low carb diet. Some evidence shows that mice survive cancers including brain cancer much longer while on high fat diets and even longer when the diets are also calorie restricted. This would tie in with the idea of intermittent fasting. Some have argued that research in this area has been slowed down because more attention is paid to lucrative cures such as expensive drugs.

Tuesday, September 18, 2007

Aerobic, Weight Training Combo Best Against Diabetes -

Aerobic, Weight Training Combo Best Against Diabetes -

MONDAY, Sept. 17 (HealthDay News) -- Most people know that exercise can help beat type 2 diabetes, but one type of fitness regimen might work best, a new study shows.

Specifically, workouts that combine aerobic and resistance training exercises appear better at controlling blood sugar than either type of activity alone, researchers say.

The finding is new, because "most other studies have looked at just one kind of exercise, either aerobic or resistance," noted lead researcher Dr. Ronald J. Sigal, an associate professor of medicine and cardiac sciences at the University of Calgary, in Alberta, Canada.

Saturday, September 15, 2007 Vitamin D can lower risk of death by 7 per cent Vitamin D can lower risk of death by 7 per cent

Vitamin D can lower risk of death by 7 per cent


From Tuesday's Globe and Mail

September 11, 2007 at 11:12 AM EDT

Taking vitamin D has been found to have a new benefit: It appears to be a life extender, according to a new study.

Researchers who pooled the results of 18 separate experiments conducted in several industrialized countries reported that people who were given a vitamin D supplement had a 7-per-cent lower risk of premature death than those who were not.

The pooled results were from experiments conducted in the United States, Germany and Britain, among other countries, and included more than 57,000 participants.

For reasons that are not yet fully understood, those who received vitamin D had a lower chance of dying prematurely than those given dummy pills, or placebos, in the experiments, said the study published yesterday in the Archives of Internal Medicine.
Related Articles

Vitamin D something of a panacea

"Mechanisms by which vitamin D supplements would decrease all-cause mortality are not clear," said the study's authors, Philippe Autier of the International Agency for Research on Cancer in Lyon, France, and Sara Gandini of the European Institute for Oncology in Milan, Italy.

Earlier research has indicated that vitamin D deficiencies are associated with higher risks of contracting major illnesses such as cancer, which account for 60 to 70 per cent of deaths in high-income countries.The study speculates that the vitamin, which is used in organs and tissues throughout the body, may cut death rates by inhibiting the proliferation of cancerous cells.

Vitamin D is also known as the sunshine vitamin, because it is produced in naked skin that is exposed to strong sunlight.

Many medical experts believe people living in northern countries have a chronic deficiency of the vitamin in winter, when the weak sunlight does not lead to creation of the nutrient in skin.

Although most of the vitamin D people have is made in their skin, it is also available in supplement form and in some foods. How big is your manager's prefrontal cortex? How big is your manager's prefrontal cortex?

How big is your manager's prefrontal cortex?


September 14, 2007

You're confident you have the right stuff. You've risen through the ranks, aced every challenge. The Myers-Briggs personality assessment indicates you have great potential as a leader of men - and women.

But hold on a sec, just one more test ... let's take a closer look at your brain, the prefrontal cortex to be precise. That's the part of the brain directly behind your forehead. Research on brain functions shows that it's a centre, not only of reasoning and problem solving, but also of personality, social interactions and planning.

And if you've got a lot of activity there, you're more likely to get high marks in school as well as rise to a position of authority on the job, a team of Canadian and American psychologists have concluded.

They say that a computer-based bank of tests that measures "executive intelligence" can predict who will excel in a managerial role, the University of Toronto reported yesterday.

Test Your Vitamin D Knowledge

Test Your Vitamin D Knowledge

Bet You Did Not Know This About Vitamin D

Vitamin D is the most common nutritional deficiency in the United States, and most physicians are clueless about its importance. If you can answer the majority of these questions correctly you are doing better than the majority of physicians.

Please remember that without question the best way to optimize your vitamin D level is with regular exposure of large portions of your skin to the sun. However, with Labor Day behind us it is time for most of us to consider switching our source of omega-3 fats from fish oil to cod liver oil, as that will supply the missing vitamin D that many of us will start lacking due to diminishing sun exposure.

This test was developed by Dr. John Cannell. He is one of the leaders in the vitamin D education movement and has a very comprehensive Web site dedicated to vitamin D. You can also subscribe to his free newsletter there.

1. Vitamin D reverses inflammatory changes associated with age-related memory impairment.

a) True

b) False

True. Researchers from Ireland were the first to demonstrate that vitamin D3 acts as an anti-inflammatory agent and turns old brains into young brains--at least as far as inflammatory cytokines are concerned. This research suggests vitamin D may prevent, or even treat, age-related cognitive decline!

Biochem Soc Trans. 2005 Aug;33(Pt 4):573-7.

2. Your blood sugar is closely associated with your vitamin D level.

a) True

b) False

True. Researchers in Australia added to the growing evidence that sun avoidance may have caused the epidemic of type 2 diabetes. The Australians' findings were straightforward and powerful. The higher your vitamin D level, the lower your blood glucose.

Clin Endocrinol (Oxf). 2005 Jun;62(6):738-41.

3. In July, a group from Minnesota found that 100 percent of elderly patients admitted for fragility fractures were vitamin-D deficient despite the fact that half of them were taking vitamin D supplements.

a) True

b) False

True. The authors found that women taking supplemental vitamin D had average levels of 16.4 ng/ml while women not taking supplements had levels of, both dangerously low. None of the 82 women got enough sun or took enough vitamin D to obtain a level of 40 ng/ml. These were fragility fractures, not fractures caused by unusual trauma. That is, their bones just sort of fell apart.

Curr Med Res Opin. 2005 Jul;21(7):1069-74.

4. Women with the lowest vitamin D levels had five times higher risk for breast cancer.

a) True

b) False

True. Women with 25(OH)-vitamin D blood levels less than 20 ng/ml were more than five times more likely to be diagnosed with breast cancer than were women with levels above 60 ng/ml. That is five, repeat five, times more likely!

Eur J Cancer. 2005 May;41(8):1164-9. Epub 2005 Apr 14.

5. Avoiding the sun doubles the risk of prostate cancer.

a) True

b) False

True. Again, the risk of avoiding the sun is clear, this time in another study with prostate cancer. However, the authors pointed out that sun exposure increases the risk of skin cancer and believed that proper vitamin D supplementation "may be the safest solution to achieve an adequate vitamin D status."

Cancer Res. 2005 Jun 15;65(12):5470-9.

I also believe supplementation is the only way to go for many people. African Americans are simply unable to spend an adequate time in the sun. In addition, the sun ages the skin and that fact alone will keep many Americans out of the sun. That said, I go into the sun whenever I can. The reason is simple: it is the most conservative thing to do. Until we know everything the sun does--and it does more than just make vitamin D--the conservative approach is to mimic our ancestors and the environment in which humans evolved, whenever we can. Therefore, it makes sense to sunbathe sensibly in the late spring, summer and early fall and take supplements or use UVB lamps the rest of the time.

6. South Korean researchers associated vitamin D deficiency with Parkinson's disease.

a) True

b) False

True. Actually, they showed that certain genetic malformations (VDR polymorphisms) are more likely in patients with Parkinson's disease, implying an association with vitamin D and Parkinsonism.

J Korean Med Sci. 2005 Jun;20(3):495-8.

7. Researchers in England discovered that patients with chronic pain have phenomenally low vitamin D levels.

a) True

b) False

True. The authors added to the evidence that severe vitamin D deficiency is associated with chronic pain. They found that 88 percent of their patients with chronic pain had levels less than 10 ng/ml. If they treated their patients, they did not report it. However, Swiss researchers recently treated chronic pain patients with vitamin D and reported the pain "disappeared" within one to three months in most of their patients. This is the second open study that showed adequate doses of vitamin D dramatically improved chronic pain.

Ann Rheum Dis. 2005 Aug;64(8):1217-9.

BMJ. 2004 Jul 17;329(7458):156-7.

Spine. 2003 Jan 15;28(2):177-9.

8. Severe vitamin D deficiency is common in TB patients.

Some English doctors don't know the difference between ideal and "normal" levels.

Most American doctors don't know the difference either.

a) All are true

b) All are false

c) Some are true and some are false

All are true. First, the authors reviewed the impressive animal evidence that vitamin D can help treat TB. Then they reported that most of their immigrant TB patients had undetectable vitamin D levels. Then they reported the normal range for their lab was between 5 to 47 ng/ml but "normal" was any level greater than 9 ng/ml. Finally, the researchers reported they treated their patients with "normal daily doses" of vitamin D, without reporting how much they gave. Apparently, they gave just enough to get patients above 9 ng/ml.

J Infect. 2005 Jun;50(5):432-7.

Keep in mind that different laboratory techniques result in different ranges for 25(OH)-vitamin D levels. No matter what technique is used, ideal levels can roughly be defined as any level above the median. In this case, as you will see below in Dr. Heaney's article, the doctors should have treated their patients with 4,000 units a day. They should also have watched for evidence of vitamin D hypersensitivity, which can occur when treating tuberculosis patients for vitamin D deficiency.

We can only mourn for the poor immigrants who have to suffer from both TB and vitamin D deficiency. Of course, few physicians in the United States know the difference between the Gaussian definition of "normal" (average ranges for the population tested) and the ideal definition of "normal" (levels above 32 ng/ml). Getting commercial reference labs to report ideal 25(OH)-vitamin D levels should be a priority of everyone involved in trying to end the epidemic of vitamin D deficiency.

9. Virtually all nephrologists give renal failure patients a vitamin D-like drug.

Virtually all renal failure patients are severely vitamin D deficient.

Some nephrologists know the difference between vitamin D and calcitriol.

a) All are true

b) All are false

c) Some are true and some are false.

All are true. Finally, the truth about renal failure patients: most of them are vitamin D deficient despite taking vitamin D analogs! Most nephrologists prescribe activated vitamin D (calcitriol) or vitamin D analogs but not vitamin D. Calcitriol and vitamin D analogs do nothing to prevent vitamin D deficiency. Renal failure patients need both vitamin D and a calcitriol-like drug. Moreover, 400 units a day of vitamin D will not correct their deficiencies. As you will see below, they need up to 4,000 units.

Am J Kidney Dis. 2005 Jun;45(6):1026-33.

P.S. If you think nephrologists know the difference between vitamin D and calcitriol, read this month's paper from some nephrologists at the University of Texas. They discuss the importance of vitamin D in preventing and treating heart disease. (I think adequate vitamin D nutrition may prevent more cardiovascular deaths than cancer deaths.) However, I read the Texas paper three times and still don't know if the authors know the difference between vitamin D and calcitriol. I hope they know the difference between cholesterol and testosterone. (Some cholesterol is metabolized into steroid hormones, vitamin D is a prehormone; testosterone is a steroid hormone, calcitriol is the most potent steroid hormone in the human body).

Kidney Int Suppl. 2005 Jun;(95):S37-42.

10. Professor Robert Heaney proved, again, that he is a gentleman and a scholar.

a) True

b) False

True. In the most important clinical paper published this month, Heaney gave the three best reasons why we should all maintain minimum levels of at least 32 ng/ml, the level that:

(a) Effectively suppresses PTH

(b) Maximizes calcium absorptio,

(c) Maximally improves glucose tolerance

Then he goes on to show that some of us, especially African Americans, will need to take 3,000 to 4,000 units every day to maintain healthy 25(OH)-vitamin D blood levels.

J Steroid Biochem Mol Biol. 2005 Jul 15.

He then defends the Institute of Medicine's (IOM) recommendation that we only take one-tenth that amount, as the best science that was available in 1997. I admire Dr. Heaney for trying to cover for the IOM. The truth is that both Dr. Heaney and Dr. Holick told the IOM that 2,000 units a day was not toxic and would prevent both adequate treatment and meaningful research. The IOM then proceeded to ignore the only two vitamin D experts on the panel.

Writing two years later, Professor Reinhold Vieth came up with dozens of studies the IOM overlooked. These studies conclusively showed 2,000 units a day could not be toxic. Furthermore, Vieth found the literature published before 1997 clearly showed 10,000 units a day was unlikely to be toxic. Vitamin D toxicity probably starts around 20,000 units a day, and then only if taken for months or even years.

Am J Clin Nutr. 1999 May;69(5):842-56.

Friday, September 14, 2007

Leptin, low-carb and hunger | Health & Nutrition by Michael R. Eades, M.D.

Leptin, low-carb and hunger | Health & Nutrition by Michael R. Eades, M.D.

The fat mass - the stored fat on the body - produces leptin, which is secreted into the blood in the circulatory system. When leptin reaches the capillaries (the tiniest blood vessels) in the brain, leptin makes its way across the BBB and into the fluid around the brain cells where it binds to the leptin receptors on the arcuate nucleus of the hypothalamus. The arcuate nucleus then sends signals to decrease food consumption and increase metabolic rate.

As the fat mass decreases in size -as it does when you don’t eat for a while and the stored fat is burned for energy - the amount of leptin in the circulation decreases as well. Less leptin crosses the BBB, less binds to the leptin receptors, and the arcuate nucleus sends out the ‘It’s time to eat’ signal. You eat and replenish the fat mass, leptin goes up, and the cycle starts again.

So as leptin levels wax and wane, so does your sense of hunger and even, to an extent, your metabolic rate.

Where does the low-carb diet fit into the picture?

There is a critical point in the cycle described above. That critical point is when the leptin crosses the BBB. If the leptin can’t get across the BBB, it can’t get to the brain. If it doesn’t get to the brain, it doesn’t shut off the hunger response irrespective of how much is circulating in the blood.

Most obese people find themselves in this very situation: high blood levels of leptin but still hungry. And eating makes more fat, which makes more leptin, which should shut off the hunger response, but it doesn’t because the ever increasing levels of leptin telling the brain to tell the obese person to quit eating don’t get to the brain to do their job.

Why not?

Research done a couple of years ago in St. Louis and in Japan pinpointed the problem. Triglycerides - fat circulating in the blood - interrupts the passage of leptin across the BBB. If trigylcerides are high, which they are in most obese people, then, basically, they block the movement of leptin into the brain. So, leptin levels are elevated in the blood, and triglycerides keep the leptin from getting to where it needs to get to shut off hunger. (click here for the abstract and full text of this research paper.)

We all know that the commonest lab finding in people following a low-carb diet is a dramatic reduction in triglyceride levels. This reduction in triglycerides allows the leptin that is already circulating in relatively large amounts to get through to the brain where it can reduce hunger. I believe that this reduction in triglycerides (which happens fairly quickly) is the primary reason that people substantially decrease their hunger on low-carb diets. And remember from the graphic above that leptin - once it gets to the brain - actually increases thermogenesis as well, which means that the metabolic rate increases.

So, the triglyceride reduction from following a low-carb diet does does double duty when more leptin gets to the brain: hunger goes down and metabolic rate goes up. That duo increases weight loss. Is it any wonder that low-carb diets virtually always manhandle low-fat diets in terms of weight loss in all of the studies in which they are compared? And it it any wonder that when people are allowed to eat an ad lib low-carb diet, they always consume fewer calories than those consuming an ad lib low-fat/high-carbohydrate diet?

Carbohydrates cause triglycerides to increase. All of Dr. Dean Ornish’s studies have shown that subjects following his ultra-low-fat/extremely-high-carbohydrate diet find their triglycerides screaming upward. It’s no wonder that most people have difficulty sticking on his diet or any low-fat/high-carb diet for very long without a lot of hand holding, behavioral therapy, meditation and the rest of his total program. People following these Ornish-like nutritional regimens are sabotaged by the elevated triglycerides that these diets cause. Consequently, they are always hungry. And sooner or later, they give in to their hunger.

leptin, hunger and triglycerides. Wonder if high triglycerides can block other things from the blood brain barrier as well. Like dopamine, or glucose or other hormones and neurotransmitters.

Technical Studies about Ketones and their Function in the Body

Technical Studies about Ketones and their Function in the Body

Effects of unbalanced diets on cerebral glucose metabolism in the adult rat.

al-Mudallal AS, Levin BE, Lust WD, Harik SI. Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Neurology 1995 Dec;45(12):2261-2265

We measured regional cerebral metabolic rates for glucose and selected cerebral metabolites in rats fed one of the following diets for 6 to 7 weeks: (1) regular laboratory chow; (2) high-fat, carbohydrate-free ketogenic diet deriving 10% of its caloric value from proteins and 90% from fat; and (3) high-carbohydrate diet deriving 10% of its caloric value from proteins, 78% from carbohydrates, and 12% from fat. In preliminary experiments, we found that moderate ketosis could not be achieved by diets deriving less than about 90% of their caloric value from fat. Rats maintained on the ketogenic diet had moderately elevated blood beta-hydroxybutyrate (O.4 mM) and acetoacetate (0.2 mM), and a five- to 10-fold increase in their cerebral beta-hydroxybutyrate level. Cerebral levels of glucose, glycogen, lactate, and citrate were similar in all groups. 2-Deoxyglucose studies showed that the ketogenic diet did not significantly alter regional brain glucose utilization. However, rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization and increased cerebral concentrations of glucose 6-phosphate. These findings indicate that long-term moderate ketonemia does not significantly alter brain glucose phosphorylation. However, even marginal protein dietary deficiency, when coupled with a carbohydrate-rich diet, depresses cerebral glucose utilization to a degree often seen in metabolic encephalopathies. Our results support the clinical contention that protein dietary deficiency coupled with increased carbohydrate intake can lead to CNS dysfunction.

High carb fucks up your brain. Low glucose metabolism in the brain is associated with ADD.

Caffeine Blocks Insulin (Possible Increased Risk for Diabetics) :: Knights of the Pain Table

Caffeine Blocks Insulin (Possible Increased Risk for Diabetics) Knights of the Pain Table

Caffeine Blocks Insulin (Possible Increased Risk for Diabetics)

A survey reported in JAMA showed that drinking coffee reduces risk for developing type II diabetes, but other studies suggest that once you have diabetes, drinking coffee may be unwise.

A report from the Netherlands showed that caffeine in coffee raises blood sugar levels. Diabetics suffer blindness, deafness, heart attacks, strokes, kidney failure, burning foot syndrome and many other serious side effects, and all are caused by a high-rise in blood sugar after meals. Anything that raises blood sugar levels too high increases cell damage in diabetics. This study shows that caffeine raises blood sugar levels by causing the body to put out large amounts of adrenalin that makes cells less responsive to insulin.

When caffeine was removed from the coffee, blood sugar levels did not rise higher than normal. On the basis of this study, diabetics should drink decaffeinated coffee, rather than one with caffeine, in addition to severely restricting sugar-added foods, bakery products, pastas, fruit juices and they should eat root vegetables and fruits only with meals.

Canadian researchers writing in Diabetes Care showed that caffeine significantly reduced insulin sensitivity. In another study in the same journal, scientists from Duke University Medical Center reported that drinking coffee could upset a diabetic’s ability to metabolize sugar.

Blood sugar levels are supposed to rise after you eat. To keep your blood sugar levels from rising too high, your pancreas releases insulin. The researchers found that taking caffeine causes blood sugar and insulin levels to rise even higher after meals. If your blood sugar rises too high, sugar sticks to cells. Once sugar is stuck on a cell membrane, it cannot be released and is converted to a poison called sorbitol which destroys that cell. High levels of insulin constrict arteries to cause heart attacks and act directly on the brain to make you hungry, on your liver to make more fat, and on the fat cells in your belly to pick up that fat. If these studies are confirmed, diabetics will be advised to restrict coffee as well as those foods that cause the highest rise in blood sugar after meals.

Caffeine can decrease insulin sensitivity in humans. Diabetes Care, 2002, Vol 25, Iss 2, pp 364-369. GB Keijzers, BE DeGalan, CJ Tack, P Smits. Smits P, Univ Nijmegen, Med Ctr, Dept Pharmacol Toxicol 233, POB 9101, NL-6500 HB Nijmegen, NETHERLANDS

Friday, September 07, 2007

Patients with type 2 diabetes show signs of vitamin D deficiency

Patients with type 2 diabetes show signs of vitamin D deficiency

"Our findings," Giovanni Targher told Reuters Health, "confirm some previous evidence demonstrating that vitamin D deficiency is highly prevalent in people with type 2 diabetes."

Because a lack of vitamin D can negatively affect bone health and have other adverse effects, he added, "widespread screening for vitamin D deficiency or routine vitamin D supplementation should be seriously considered" for people with diabetes.

Targher, at Sacro Cuore Hospital, Negrar, and his colleagues studied blood levels of vitamin D in 459 individuals with type 2 diabetes and a comparison group of 459 matched non-diabetic "controls."

The rate of vitamin D deficiency (61 percent) was significantly higher in the diabetics than in the controls (43 percent). Diabetics with vitamin D deficiency were more likely to be women, to have poorly controlled diabetes, and to be taking insulin and cholesterol-lowering drugs.

In all, 31 percent of the diabetics had cardiovascular disease, which was strongly associated with low vitamin D levels.

More studies are "obviously necessary to determine whether vitamin D deficiency predicts (the occurrence of) cardiovascular disease," Targher added, "and to determine whether vitamin D supplementation would be protective against cardiovascular disease."

Toledo Free Press - We have underestimated the importance of Vitamin D

Toledo Free Press - A tradition for Toledo's future

Vitamin D is important for several reasons. A deficiency in vitamin D causes rickets and prevents children from reaching their peak bone mass. In adults, the lack of vitamin D contributes to osteoporosis and the painful bone disease osteomalacia.

We have suspected for a long time that vitamin D deficiency might also cause heart disease. A New Zealand study reported in 1990 showed that heart attack victims had lower levels of vitamin D in their bodies than people who did not have heart attacks. A 1998 study showed that heart attacks increased by 53 percent during winter months when sunlight is less available.

More recent studies have found that adequate levels of vitamin D helps reduce inflammation, lower blood pressure and improve insulin sensitivity. These variables all decrease the risk of heart disease. A study of Japanese dialysis patients indicates that returning the patients vitamin D to appropriate levels reduced heart attacks and death from heart disease.

Study: Vitamin D May Prevent Some Cancers, Sun-Related Vitamin Might Prevent Many Cases Of Colon And Breast Cancer - CBS News

Study: Vitamin D May Prevent Some Cancers, Sun-Related Vitamin Might Prevent Many Cases Of Colon And Breast Cancer - CBS News

(CBS) A new study suggests the number of cases of colon and breast cancer could be cut dramatically if people got more vitamin D.

University of California researchers estimate 250,000 cases of colon cancer and 350,000 cases of breast cancer could be prevented worldwide by increasing intake of vitamin D. Sunlight spurs production of vitamin D in the skin, and people who don't get much sun exposure tend to have lower levels of the vitamin.

Past research indicated that vitamin D helps slow the growth and spread of cancer cells.

"There's been a lot of evidence for a long time that vitamin D is very important, not just for bones, which everybody knows, but for all the organs in the body," Dr. Larry Norton, an oncologist at New York's Memorial Sloan-Kettering Cancer Center, explained to Early Show co-anchor Harry Smith Thursday.

"What's very interesting," he continued, "is that all humans really can (trace) their ancestry to just a few thousand people who walked out of Africa into what is now Yemen, just about 80,000 years ago, and populated the whole earth.

"As people moved further north, their skin got lighter. Why? So it could absorb more vitamin D from sunlight. But now, in the modern world, we wear clothes, we wear sunblock, we work indoors most of the time - so, essentially, nobody who lives outside the equator gets enough vitamin D, especially in the winter months.

"This study was interesting because it looked at sun exposure, cloud cover, as well as vitamin D levels in over 170 countries. And there's a clear association with less sun, lower vitamin D levels and higher incidences of certain cancers, particularly colon cancer and breast cancer."

Thursday, September 06, 2007

Lean plate club: Science asks: Is food addictive?

Lean plate club: Science asks: Is food addictive?

Lean plate club: Science asks: Is food addictive?

Research is still scanty, but the evidence that exists "is extremely interesting and provocative."

By Sally Squires, Washington Post

Alcohol, nicotine and cocaine are just a few of the substances known to be addictive. Now some scientists wonder if food should be added to the list.

"Are there certain things in food that act on the brain and set up a classic addictive process, like tolerance, withdrawal and craving?" asks psychologist Kelly Brownell, who organized a recent scientific meeting on food addiction at Yale University. While the research is still scanty, the evidence that exists "is extremely interesting and provocative and suggests to me that something is there," Brownell says.

That's not news to many Lean Plate Club members who e-mailed me recently about their food struggles. Most asked not to be named, reflecting how they feel stigmatized by behaviors they have trouble controlling.

"I feel addicted to food at times," one wrote. "Food is like a drug to me. It can change my emotional state. For many years, I have 'used' food as a feel-good panacea, self-medicating with warm chocolate chip cookies or a pint of Chunky Monkey. I will sit down with a food I like in an upset state of mind and will eat it all immediately, beyond the feeling of fullness. It's like a compulsion to finish the entire thing."

Another member described how "thinking about food is like a pounding obsession -- a hammer beating in my head that is driving no nail. ... I hate feeling full. I'm not in control and I hate letting this demon take over me. I want to stop and nobody has any idea."

Those descriptions certainly sound like the feelings that doctors associate with addiction. But whether they stem from the same physiological changes that occur with drug and alcohol dependency is not yet known. "Is it an addiction to food or an addiction to eating?" asks Susan Yanovski, director of the obesity and eating disorders division at the National Institute of Diabetes and Digestive and Kidney Diseases. "Or is it another manifestation of a compulsive behavior like gambling or shopping?"

The brain and food

Brain imaging may soon provide answers. At Brookhaven National Laboratory, psychiatrist Dr. Nora Volkow and her colleagues map dopamine receptors on brain cells. This powerful neurotransmitter plays a key role in addiction. Dopamine systems are disrupted by addictive drugs, from alcohol to methamphetamine, which hijack the control of volition and the quest for rewards.

It turns out that food also affects the brain's dopamine systems. When Volkow, who is also director of the National Institute on Drug Abuse, compared brain images of methamphetamine users with those of obese people, she found both groups had significantly fewer dopamine receptors than healthy people. Even more interesting: the higher the body mass index, the fewer the dopamine receptors -- opening the door to a better understanding of why it can be so difficult for some people to lose weight and keep it off.

What role dopamine may play in obesity -- and how eating affects it -- is still to be determined. No one knows if the brain changes occurred before or after people became obese, or if they can be reversed with weight loss. Are some people more susceptible to certain popular foods such as sugary, high-fat fare? Might food additives, preservatives and other substances have an effect on dopamine receptors?

"It's a fascinating topic, but I don't think that it's ready for prime time in terms of suggesting intervention or suggesting that this [food addiction] is a real phenomenon," Yanovski says.

Even if food prompts feelings and behaviors in some people that are like addiction, there are likely to be many treatment challenges ahead. "You can be totally abstinent in using drugs or alcohol, but you can't be abstinent with eating," Yanovski notes.

That's why some people who feel that they've been snared by food addictions sometimes try to eliminate the specific foods that seem to trigger their overeating. "My name is Lisa and I am a compulsive eater," wrote one Lean Plate Club member who has eliminated refined, processed foods high in sugar, white flour, artificial sweeteners and food additives from her diet. "I am addicted to food, and for me, to attempt to eat certain foods in moderation is no different than suggesting that a crack addict or alcoholic smoke crack or drink alcohol in moderation. It simply is not possible."

Other Lean Plate Club members view chronic overeating as a symptom of a bigger problem. "Compulsive eating to me is a sign that my soul is hungry for something else," wrote one. "I try to think of it as a sign that I need to change something in my life. When I think of it as a tool for self-knowledge, it becomes a gift and much more manageable."

Monday, September 03, 2007

Life Enhancement:: Skipping Meals Regularly May Be Good for Your Health

Life Enhancement:: Skipping Meals Regularly May Be Good for Your Health

Overweight and Obesity Are Epidemic

We must eat to live. The problem is that many people live to eat. Our seemingly insatiable appetite has spawned an explosion of obesity, particularly in the United States, where the rate increased by 61% between 1991 and 2000.1 It’s now thought that 25–30% of all adults in the USA are obese. If we include overweight individuals (those with a body mass index greater than 25), then 56% of American adults are overweight or obese. Since many studies have shown that these conditions contribute significantly to such devastating diseases as cancer, cardiovascular disease, type 2 (adult-onset) diabetes, and Alzheimer’s disease, our excessive food consumption, particularly of high-calorie foods, is a deadly addiction.

Obesity Links Diabetes and Alzheimer’s

At first glance, the notion that diabetes and Alzheimer’s disease could have a common cause might seem preposterous. After all, isn’t diabetes a disease in which high glucose levels and decreased insulin sensitivity contribute to a myriad of severe health problems, whereas in Alzheimer’s there is a degeneration of brain neurons resulting eventually in total mental incapacity? Well, yes—but scientists are coming up with some intriguing hypotheses that tie these two modern epidemics together.

Obesity is by far the greatest risk factor for type 2 diabetes, and the link is very strong: for every kilogram of increase in self-reported weight, the risk of diabetes increases approximately 9%, and as we grow ever fatter in the United States, the number of diabetics is rising rapidly, with a 33% increase seen between 1990 and 1998.2

AGEs and Free Radicals Will Do You Harm

One of the many harmful conditions associated with type 2 diabetes is the excessive accumulation of advanced glycation end products, or AGEs. These sugar/protein complexes accumulate in the blood and tissues of all of us as we age, and some researchers believe that they’re implicated in the pathogenesis of such modern epidemics as heart disease and Alzheimer’s disease.3 Their link with diabetes stems from the fact that elevated blood glucose levels, which are a characteristic of that disease, promote the rapid formation and accumulation of AGEs.

Another way in which the effects of obesity may link diabetes and Alzheimer’s is through the increased production of free radicals, destructive molecules that are produced inside brain neurons and all the other cells in the body when the cells generate energy from their primary source of fuel, glucose. In high concentrations, free radicals can cause serious problems, including DNA damage and the oxidation of proteins and lipids. Studies have shown that cellular signs of excessive free radical damage are significantly higher in people who are obese.4

Caloric Restriction Extends Lifespan

A simple (but far from easy) way to decrease your weight and avoid the major health problems of obesity is to eat less, thereby taking in fewer calories. In fact, a significant body of evidence shows that long-term dietary caloric restriction of 30% or more (i.e., taking in at least 30% fewer calories than normal) can slow the aging process and maintain health and vitality in a great variety of species, from simple invertebrates to primates.5 Such extreme caloric restriction (CR), in fact, is the only environmental variable that has been shown to markedly slow the rate of aging over a wide range of species.

Most significantly, CR can extend lifespan, by up to 50% in some cases. Exactly how this is accomplished is not known, but tantalizing clues are found in several biomarkers of aging. In primates, CR has been shown to decrease plasma glucose and insulin levels, increase insulin sensitivity, decrease cholesterol and triglyceride levels, lower blood pressure, and increase DHEA levels. Another notable effect of a CR diet is, not surprisingly, major weight loss, resulting in an extremely lean physique—no excess body fat.


Intermittent Fasting—A Shortcut to Major Health Benefits

Although caloric restriction seems to be the way to live a longer, healthier life, a reality check suggests that few, if any, people would ever do it—there are just too many tempting foods out there, and a lifetime of voluntary food deprivation doesn’t sound too appealing. But wait—some exciting research has just been published indicating that it might be possible to obtain the health benefits of a CR diet without actually having to go on one.


Researchers at the National Institute on Aging in Baltimore have found that, in laboratory mice, a long-term (20-week) program of intermittent fasting—a total fast every other day, interspersed with unlimited food every other day—conferred virtually all the health benefits of a CR diet, and it did so with little or no attendant weight loss (which could be a plus or a minus in humans, depending on what level they were starting from).6*

*In previous studies of a similar kind with mice and rats, the IF animals usually lost weight, but the strain of mice used in this particular study did not.

The researchers did not record the effects of intermittent fasting on longevity, because the nature of the study required that the mice be killed so their brains could be microscopically examined. In two previous studies well over a decade ago, however, it was found that the same kind of intermittent fasting regimen in the same strain of mice did result in significant extensions of lifespan.7,8


Intermittent Fasting Reduced Glucose and Insulin Levels

By the end of the study, the IF mice were consuming essentially the same amount of food as the AL mice, simply by eating twice as much food on their “on” days as the AL mice ate every day. Meanwhile, the LDF mice ate 40% less food than the AL mice, and they lost 49% of their weight (they were very skinny and hungry—but healthy—mice).

Blood tests done after 14 weeks (and following a 14-hour fast for all the mice) showed that the concentrations of glucose and insulin were significantly decreased in both the IF mice and the LDF mice—which is good! Remarkably, in fact, they were lower in the IF mice—this despite the fact that the IF mice ate the same amount of food as the AL mice, which did not show a significant decrease in their glucose and insulin levels and thus continued to be good candidates for diabetes in the long run.

It could be expected that binge eating, such as that indulged in by the IF mice every other day, would have some negative health effects, notably the excessive generation of free radicals or of AGEs (advanced glycation end products, remember?). Remarkably, however, it seems that these potentially harmful effects were more than offset by the evident benefits of alternate-day fasting. As the authors put it:
Apparently, confining bouts of high caloric intake to a limited time window with long intervening periods of fasting results in adaptive responses that do not occur when meals are more frequent. . . . It may be that alternating periods of anabolism [the metabolic buildup of complex biomolecules] and catabolism [the metabolic breakdown of complex biomolecules] play a mechanistic role in triggering increases in cellular stress resistance and the repair of damaged biomolecules or cells.
Intermittent Fasting Protected Brain Neurons

After 24 weeks, the researchers injected the brains of the mice with a substance, kainic acid, that causes neurological damage similar to that seen in the brains of Alzheimer’s victims. The damage was induced in the hippocampus, a part of the brain that is associated with memory and learning and that is characteristically impaired in Alzheimer’s disease. Then, 24 hours later, the mice were killed and their brains examined.

The AL brains showed major pathological changes, as expected. In the LDF brains, by comparison, there was a significant increase in the survival of hippocampal neurons, and remarkably, the neuronal survival rate was even higher in the IF brains than in the LDF brains. This seems to show that intermittent fasting is neuroprotective, independently of overall caloric intake—and that too is remarkable.

Lose Weight and Live Better and Longer

Since it is known that caloric restriction extends lifespan in a wide variety of animals and that intermittent fasting, which confers essentially the same health benefits as CR, can extend lifespan in mice, one is tempted to think that IF might also extend lifespan in humans—provided, of course, that they made a lifetime practice of it. It’s also intriguing to speculate whether a less rigorous regimen, such as skipping one meal (or even two) every other day, or eating only two meals a day instead of three, might have some health benefits. It’s hard to say, but the chances seem good, and it’s almost certain to do no harm.

In any case, one thing is for sure: combating overweight and obesity so as to maintain a healthy weight and keep your blood glucose and insulin levels (not to mention cholesterol levels) well under control is one of the best things you can possibly do for your health and your prospects for a long and happy life.