Saturday, June 30, 2007

A Case Against Cardio (from a former mileage king)

Mark’s Daily Apple A Case Against Cardio (from a former mileage king)

A Case Against Cardio (from a former mileage king)

We all know that we need to exercise to be healthy.

Unfortunately, the popular wisdom of the past 40 years – that we would all be better off doing 45 minutes to an hour a day of intense aerobic activity – has created a generation of overtrained, underfit, immune-compromised exerholics. Hate to say it, but we weren’t meant to aerobicize at the chronic and sustained high intensities that so many people choose to do these days. The results are almost always unimpressive. Ever wonder why years of “Spin” classes, endless treadmill sessions and interminable hours on the “elliptical” have done nothing much to shed those extra pounds and really tone the butt?

Don’t worry. There’s a reason why the current methods fail, and when you understand why, you’ll see that there’s an easier, more effective – and fun - way to burn fat, build or preserve lean muscle and maintain optimal health. The information is all there in the primal DNA blueprint, but in order to get the most from your exercise experience, first you need to understand the way we evolved and then build your exercise program around that blueprint.

[...]

Humans, like all mammals, evolved two primary energy systems that powered the skeletal muscles of our hunter-gatherer ancestors 40,000 years ago and that would keep us all well-powered the same way today, if we weren’t so bent on circumventing them with our ill-fated (literally) lifestyle choices.

The first energy system relied heavily on the slow burning of fats, keeping us fueled while we were at rest or sleeping, yet also allowing for continuous or intermittent low levels of aerobic activity (think of our ancestors walking across the savannah for hours foraging for roots, shoots, berries, grubs, insects and the occasional small animal). It makes sense. Fats are very efficient fuels that are stored easily in the fat cells and burn easily and cleanly when lots of oxygen is present (as when we are breathing normally). Even if there’s no food in the immediate area, a well-trained fat-burning hunter-gatherer could continue walking and foraging for days without compromising his or her health or efficiency.

The second major energy system we developed through evolution was an ATP-fueled system that allowed for intense loads of work to be done in very brief bursts (think of our hunter-gatherer ancestors sprinting to the safety of a tree to avoid being eaten by a lion). ATP is always sitting right there within the muscle cells, available in a split second, and it is the highest octane fuel we have. In fact, it’s ATP and adrenaline that allow the little old lady to lift the front end of the Ford Fairlane off her husband when the jack fails. Unfortunately, the muscles can only store about 20 seconds worth of this precious fuel to complete life-or-death tasks. If our ancestors survived that quick sprint to safety, their ATP reserves were filled again within minutes using the other energy systems.

Furthermore, that brief burst of intense energy sparked a small “growth spurt” in the muscle, making it even stronger for the next encounter with the next lion – a true survival adaptation.

(Note: While our energy systems are actually quite complex, varied and interrelated, I have simplified things here to make it easier to “digest”.)

Bottom line: Fats and ATP were the two primary energy sources for locomotion: we either moved slowly and steadily or “fight or flight” fast, and we became stronger and healthier the more we used only those energy systems.

But here’s the real take-home message for us: We did not evolve to rely heavily on a carbodydrate-fueled energy system, and yet, carbohydrate metabolism seems to rule our lives today. Yes, carbohydrate (in the form of glucose) can play a major role in the production of energy in skeletal muscle, but it turns out that the heart and skeletal muscle prefer fatty acids (fat) as fuel over glucose.

Friday, June 29, 2007

Thursday, June 28, 2007

Central Intelligence Agency's Strangeloves altered mind of a girl aged 4

The Australian: Agency's Strangeloves altered mind of a girl aged 4 [ 28jun07 ]

Agency's Strangeloves altered mind of a girl aged 4
Robert Lusetich, Los Angeles correspondent
28jun07

EASILY lost, on page 425, in the mass of the CIA's notorious "Family Jewels" files is a short paragraph outlining "potentially embarrassing Agency activities".


"Experiments in influencing human behaviour through the administration of mind- or personality-altering drugs to unwitting subjects."

Of all the heinous acts committed by the CIA in the name of national security, these experiments, done on the agency's behalf by prominent psychiatrists on innocent victims - including children as young as four - may be the darkest.

"We have no answer to the moral issue," former director Richard Helms infamously said when asked about the nature of the projects.

The release of the Family Jewels documents revealed the CIA handsomely funded these real-life Dr Strangeloves and engaged pharmaceutical companies to help its experiments.

The agency appealed to Big Pharma to pass on any drugs that could not be marketed because of "unfavourable side effects" to be tested on mice and monkeys. Any drugs that passed muster would then be used, according to an internal memo, on volunteer US soldiers.

The Family Jewels files do not provide further detail into the numerous mind-control programs, such as MKULTRA, covertly propped up by the agency. In 1953, MKULTRA was given 6per cent of the total CIA budget without any oversight.

Only the tip of a large iceberg had been previously released by the CIA under Freedom of Information Act provisions.

Yesterday's acknowledgments will comfort those who have long campaigned for truth and restitution.

The nature of the experiments, gathered from government documents and testimony in numerous lawsuits brought against the CIA, is shocking, from testing LSD on children to implanting electrodes in victims' brains to deliberately poisoning people with uranium.

First artificial life 'within months' | International News | News | Telegraph

First artificial life 'within months' | International News | News | Telegraph

Scientists could create the first new form of artificial life within months after a landmark breakthrough in which they turned one bacteria into another.


Craig Venter likened the process to 'changing a Macintosh computer into a PC by inserting a new piece of software'

In a development that has triggered unease and excitement in equal measure, scientists took the whole genetic makeup - or genome - of a bacterial cell and transplanted it into a closely related species.

This then began to grow and multiply in the lab, turning into the first species in the process.

The team that carried out the first “species transplant” says it plans within months to do the same thing with a synthetic genome made from scratch in the laboratory.

If that experiment worked, it would mark the creation of a synthetic lifeform.

The scientists want to create new kinds of bacterium to make new types of bugs which can be used as green fuels to replace oil and coal, digest toxic waste or absorb carbon dioxide and other greenhouse gases from the atmosphere.

But this pioneering research also triggers unease about the limits of science and the inevitable fears about “playing god,” as well as raising the spectre that this technology could one day be abused to create a new generation of bioweapons.

Producing living cells from synthetic genomes of lab-made DNA would require the ability to move and manipulate whole genomes.

To that end, a milestone was passed today by a team led by Craig Venter, the first person to have his entire genetic makeup read, and which included the Nobel prizewinner Ham Smith.

Dr Venter said that, in the light of this success, the culmination of a decade’s work, he will be attempting the first transplant of a lab-made genome to create the first artificial life “within months.”

Dr Venter said: “We would hope to have the first fuel from synthetic organisms certainly within the decade, possibly within half that time.”

Working Out Your Brain | GNIF Brain Blogger

Working Out Your Brain | GNIF Brain Blogger

In nature’s original design plan, the brain was the leader for coordinating our physical activities: the “motor high-command.” It comes as little surprise then, that exercise strengthens the brain’s interconnections, and rejuvenates the mind.

The chemical link between the mind and body is best exemplified by the brain derived neurotrophic growth factor (BDNF), a protein found in our brain which helps brain cells to stay healthy, sprout new connections, and develop plasticity (the ability to form new connections between cells). Previous experiments have shown that short-term and long-term exercise both lead to a release of BDNF from various parts of our brain, more so from the cortex, basal forebrain and hippocampus, which are areas considered vital for learning, higher thinking, and memory.

A new study, published in Medicine & Science in Sports & Exercise, the official journal of the American College of Sports Medicine, actually confirms that the more intense the exercise, the more amount of BDNF released. The study, carried out at the Texas Tech University, recruited two groups of 15 cyclists who were assigned “heavy” and “light” graded intensity exercises. Their serum BDNF and mental cognition were measured before and after the test. While heavy exercises were associated with both increased BDNF levels and improved cognition test scores, the study has not conclusively demonstrated that the improvement in mental function due to heavy exercise is linked exclusively to increased BDNF release. According to Lee Ferris and James Williams, authors of the paper, the study could be underpowered (low numbers of cyclists), and future studies with larger numbers of participants could prove the definitive link.

Men with ADD / ADHD Paul's Story

Men with ADD / ADHD Paul's Story

Paul's Story

Im a 43 year old male. I was diagnosed with ADD about six months ago. Ive always been challenged to stay focused and organized, but never considered ADD because I wasnt hyper or disruptive as a child. It seems a common misconception with ADD, is that it necessarily includes excessive, and usually, distracting levels of energy. Rather than being fed with the energy some describe with ADD, Im frequently exhausted and overwhelmed by details and unfinished projects.

My office is typically piled with unfiled papers and half finished projects. After a few months the clutter drives me crazy, so I completely ignore everything else to get organized, promising myself that I wont let this happen again. It would be so much simpler to spend a few minutes each day keeping organized. Inevitably, within a week, the piles return.

I go to work each day, knowing what needs to be accomplished, but frequently overwhelmed by simple tasks such as making a necessary phone call, or returning a simple email. As the day progresses, thoughts of unfinished projects pop into my head, and I get discouraged by my inability to take care of them. Perhaps Ive lived so many years fighting to finish projects, that Im afraid to start new ones. When I finish a project, I look back at its simplicity, and recognize that it could have taken an hour, but I spent three days on it.

My biggest challenge is maintaining organization with finances. A few years ago, I needed to reallocate some retirement investments. I knew my current portfolio was declining. The statements came each month, I needed to spend a few minutes to look them over, then make a phone call to move the funds to alternative investments. It seems simple, but I spent months paralyzed, and for some reason unable to make that simple phone call. I lost more than $40,000, when a few minutes of my time could have easily maintained the value of the investment.

Ten years ago, I was diagnosed with a chronic form of mild depression (Dythsymia). Upon diagnosis, I recognized that I had lived with the depression for decades without knowing it. Ive responded reasonably well to medication, and I recognize that Ill probably need medication for the rest of my life. While anti depressants have lightened the grey cloud, focus, motivation, and organization have remained a challenge. Ive read that ADD and depression frequently co-exist.

My 13 year old son was diagnosed with ADD last year. He takes Concerta, and it has made a remarkable difference in his ability to function in school. One morning I tried the Concerta. I was astounded at the difference it made. I accomplished more that day than I had in the previous week. Rather than feeling overwhelmed, I was energized and focused. To make a long story short, Im receiving medical treatment for depression as well as ADD. Ive found that the Concerta becomes less effective after several days of consistent use. I try not to rely on it each day. I usually take Concerta 3-4 times a week.

Although Ive benefited from medical treatment, I worry about the long term effect of medications, particularly ADD medications. I hope to find non medicinal treatments. Diet and exercise make a difference, but havent been completely effective. The ADD medication has made a significant difference, but I dislike scheduling my productivity. While anti depressants maintain a steady state of effectiveness day after day, the ADD medications provide a distinct time window of productivity. Its like the lights suddenly go out, and Im left hanging and fighting to get through the rest of the day.

In spite of the challenges, I obtained a college degree, and Ive maintained a reasonably successful career. My wife has been remarkably patient, and were raising four bright, energetic children. With patience and understanding, Im learning to recognize and acknowledge the challenges that come with depression and ADD, without giving in to them. It has taken a long time for me to admit that these disorders are real. I wasted many years in denial, thinking I could fix everything with a better attitude. That was an expensive mistake, and a waste of precious time. Treatment is helping me be a much better husband, father, employee and friend. Dont be afraid to find help. I hope this helps someone. Dont give up.

There are a number of great stories at this site from ordinary people with ADD.

Wednesday, June 27, 2007

Effects of a Low-Glycemic Load vs Low-Fat Diet in Obese Young Adults: A Randomized Trial

JAMA -- Abstract: Effects of a Low-Glycemic Load vs Low-Fat Diet in Obese Young Adults: A Randomized Trial, May 16, 2007, Ebbeling et al. 297 (19): 2092

Results Change in body weight and body fat percentage did not differ between the diet groups overall. However, insulin concentration at 30 minutes after a dose of oral glucose was an effect modifier (group x time x insulin concentration at 30 minutes: P = .02 for body weight and P = .01 for body fat percentage). For those with insulin concentration at 30 minutes above the median (57.5 µIU/mL; n = 28), the low–glycemic load diet produced a greater decrease in weight (–5.8 vs –1.2 kg; P = .004) and body fat percentage (–2.6% vs –0.9%; P = .03) than the low-fat diet at 18 months. There were no significant differences in these end points between diet groups for those with insulin concentration at 30 minutes below the median level (n = 28). Insulin concentration at 30 minutes after a dose of oral glucose was not a significant effect modifier for cardiovascular disease risk factors. In the full cohort, plasma high-density lipoprotein cholesterol and triglyceride concentrations improved more on the low–glycemic load diet, whereas low-density lipoprotein cholesterol concentration improved more on the low-fat diet.

Conclusions Variability in dietary weight loss trials may be partially attributable to differences in hormonal response. Reducing glycemic load may be especially important to achieve weight loss among individuals with high insulin secretion. Regardless of insulin secretion, a low–glycemic load diet has beneficial effects on high-density lipoprotein cholesterol and triglyceride concentrations but not on low-density lipoprotein cholesterol concentration.

Conclusion: If you are overweight and insulin resistant (have fat around the belly)- low carb is the way to go! HDL and triglycerides are huge risk factors, and low carb is the way to improve them.

Tuesday, June 26, 2007

Tanning is associated with optimal vitamin D status (serum 25-hydroxyvitamin D concentration) and higher bone mineral density -- Tangpricha et al. 80 (6): 1645 -- American Journal of Clinical Nutrition

Tanning is associated with optimal vitamin D status (serum 25-hydroxyvitamin D concentration) and higher bone mineral density -- Tangpricha et al. 80 (6): 1645 -- American Journal of Clinical Nutrition

ABSTRACT
TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES


Background: Vitamin D is made in the skin on exposure to solar radiation, and it is necessary to optimal skeletal health. Subjects who use a tanning bed that emits ultraviolet B radiation (290–315 nm) are likely to have higher 25-hydroxyvitamin D [25(OH)D] concentrations than do subjects who do not regularly use a tanning bed.

Objective: The first objective of this study was to ascertain whether subjects who regularly use a tanning bed have higher 25(OH)D concentrations than do subjects who do not use a tanning bed. The second objective was to ascertain whether higher 25(OH)D concentrations correlated positively with bone mineral density.

Design: This cross-sectional analysis examined 50 subjects who used a tanning bed at least once a week and 106 control subjects. Each subject gave a blood specimen for measurement of serum 25(OH)D and parathyroid hormone concentrations. Each subject underwent bone mineral density testing of the hip and spine.

Results: Subjects who used a tanning bed had serum 25(OH)D concentrations 90% higher than those of control subjects (115.5 ± 8.0 and 60.3 ± 3.0 nmol/L, respectively; P < 0.001). Subjects who used a tanning bed had parathyroid hormone concentrations 18% lower than those of control subjects (21.4 ± 1.0 and 25.3 ± 0.8 pg/mL, respectively; P = 0.01). Tanners had significantly higher BMD and z scores at the total hip than did nontanners. Conclusion: The regular use of a tanning bed that emits vitamin D–producing ultraviolet radiation is associated with higher 25(OH)D concentrations and thus may have a benefit for the skeleton. Key Words: Vitamin D deficiency • secondary hyperparathyroidism • vitamin D • bone mineral density • bone mineral content • tanning

[...]

Adults who used a tanning bed had 90% higher serum 25(OH)D and 18% lower PTH concentrations than did adults who did not use a tanning bed. The prevalence of vitamin D deficiency [25(OH)D 50 nmol/L] was significantly lower in the tanners (8%) than in the nontanners (41.5%) at the end of the winter. Tanners also had significantly higher BMD at the hip than did the nontanners, which confirms the findings of Bischoff et al (8). There was a small but nonsignificant positive relation between serum 25(OH)D concentrations and BMD at the hip and spine. These findings have important clinical implications. The increased public awareness of the negative effect of sunlight in causing skin cancer has resulted in the fact that many adults and children always wear sun protection or completely avoid sunlight exposure. A lack of sunlight exposure can result in vitamin D deficiency. Humans produce most of the vitamin D found in the circulation in the skin through exposure to sunlight (2, 3), and adults who spend most of their time indoors are at risk of vitamin D deficiency (15–18, 20, 21, 23–26). Nursing home residents, medical inpatients, institutionalized persons, and blacks are at highest risk of vitamin D deficiency (18, 23–28). Subjects living in northern latitudes have low production of vitamin D in the skin because even the zenith of the angle of the sun's rays does not allow for cutaneous vitamin D3 production (2, 3, 15, 17, 28). In addition, increased pigmentation (27–29) or the wearing of clothing that largely covers the body (30–32) impairs the production of vitamin D3 in the skin. The regular use of sunscreens can also result in vitamin D deficiency (33): sunscreen with an SPF > 8 can reduce the production of vitamin D in the skin by as much as 95% (2, 14).

Young adults are also at risk of vitamin D deficiency because of inadequate sunlight exposure that results from greater pursuit of indoor activities, greater use of sunscreen because of fear of skin cancer (34, 35), and less consumption of vitamin D–fortified milk (15, 36, 37) than were seen in previous generations. A recent survey of young adults living in Boston found that 36% of young adults were vitamin D deficient, even though many took a multivitamin and drank a glass of milk daily (15). African American adolescents and white preteen girls are also at risk for vitamin D deficiency (37, 38).

Vitamin D is important to bone mineralization because of its role in the maintenance of adequate serum calcium and phosphorus concentrations (2, 3). Vitamin D deficiency results in osteomalacia in adults and is a frequent source of occult muscle and bone pain (39–41). There is increasing evidence that vitamin D can protect against the development of many chronic diseases, including type 1 diabetes mellitus, hypertension, cardiovascular disease, common cancers, multiple sclerosis, and rheumatoid arthritis (2, 3).

The use of tanning beds has been promoted to the public for the cosmetic purpose of tanning, but this study shows that a moderate use of tanning beds may also provide some medical benefit. Higher concentrations of 25(OH)D throughout the year may have a significant effect in enhancing intestinal calcium absorption and improving bone health (7, 8, 42). Blood concentrations of 25(OH)D in tanners are > 75 nmol/L, which is considered to be necessary for maximum intestinal calcium transport (23, 42). This may explain why higher serum 25(OH)D concentrations are associated with higher bone density. There is mounting evidence that a healthy concentration of 25(OH)D (ie, >75 nmol/L) may reduce the risk of colon, breast, and prostate cancers, hypertension, and autoimmune diseases (2, 3, 39–42).

In conclusion, the regular use of a tanning bed results in higher 25(OH)D concentrations and prevents increased seasonal prevalence of vitamin D deficiency during the winter. The subjects who had used tanning beds for a mean of 5 y had higher BMD at the hip than did the nontanners (control subjects). Larger studies should be conducted to investigate the potential positive effect of chronic use of tanning beds on vitamin D status and bone health.

Basic Nutrition: The Miracle of Vitamin D

Basic Nutrition: The Miracle of Vitamin D

Vitamin D From Sunlight

Pick up any popular book on vitamins and you will read that ten minutes of daily exposure of the arms and legs to sunlight will supply us with all the vitamin D that we need. Humans do indeed manufacture vitamin D from cholesterol by the action of sunlight on the skin but it is actually very difficult to obtain even a minimal amount of vitamin D with a brief foray into the sunlight.4,5

Ultraviolet (UV) light is divided into 3 bands or wavelength ranges, which are referred to as UV-C, UV-B and UV-A.6 UV-C is the most energetic and shortest of the UV bands. It will burn human skin rapidly in extremely small doses. Fortunately, it is completely absorbed by the ozone layer. However, UV-C is present in some lights. For this reason, fluorescent and halogen and other specialty lights may contribute to skin cancer.

UV-A, known as the "tanning ray," is primarily responsible for darkening the pigment in our skin. Most tanning bulbs have a high UV-A output, with a small percentage of UV-B. UV-A is less energetic than UV-B, so exposure to UV-A will not result in a burn, unless the skin is photosensitive or excessive doses are used. UV-A penetrates more deeply into the skin than UV-B, due to its longer wavelength. Until recently, UV-A was not blocked by sunscreens. It is now considered to be a major contributor to the high incidence of non-melanoma skin cancers.7 Seventy-eight percent of UV-A penetrates glass so windows do not offer protection.

The ultraviolet wavelength that stimulates our bodies to produce vitamin D is UV-B. It is sometimes called the "burning ray" because it is the primary cause of sunburn (erythema). However, UV-B initiates beneficial responses, stimulating the production of vitamin D that the body uses in many important processes. Although UV-B causes sunburn, it also causes special skin cells called melanocytes to produce melanin, which is protective. UV-B also stimulates the production of Melanocyte Stimulating Hormone (MSH), an important hormone in weight loss and energy production.8

The reason it is difficult to get adequate vitamin D from sunlight is that while UV-A is present throughout the day, the amount of UV-B present has to do with the angle of the sun's rays. Thus, UV-B is present only during midday hours at higher latitudes, and only with significant intensity in temperate or tropical latitudes. Only 5 percent of the UV-B light range goes through glass and it does not penetrate clouds, smog or fog.

Sun exposure at higher latitudes before 10 am or after 2 pm will cause burning from UV-A before it will supply adequate vitamin D from UV-B. This finding may surprise you, as it did the researchers. It means that sunning must occur between the hours we have been told to avoid. Only sunning between 10 am and 2 pm during summer months (or winter months in southern latitudes) for 20-120 minutes, depending on skin type and color, will form adequate vitamin D before burning occurs.9

It takes about 24 hours for UV-B-stimulated vitamin D to show up as maximum levels of vitamin D in the blood. Cholesterol-containing body oils are critical to this absorption process.10 Because the body needs 30-60 minutes to absorb these vitamin-D-containing oils, it is best to delay showering or bathing for one hour after exposure. The skin oils in which vitamin D is produced can also be removed by chlorine in swimming pools.

The current suggested exposure of hands, face and arms for 10-20 minutes, three times a week, provides only 200-400 IU of vitamin D each time or an average of 100-200 IU per day during the summer months. In order to achieve optimal levels of vitamin D, 85 percent of body surface needs exposure to prime midday sun. (About 100-200 IU of vitamin D is produced for each 5 percent of body surface exposed, we want 4,000 iu.) Light skinned people need 10-20 minutes of exposure while dark skinned people need 90-120 minutes.11

Latitude and altitude determine the intensity of UV light. UV-B is stronger at higher altitudes. Latitudes higher than 30° (both north and south) have insufficient UV-B sunlight two to six months of the year, even at midday.12 Latitudes higher than 40° have insufficient sunlight to achieve optimum levels of D during six to eight months of the year. In much of the US, which is between 30° and 45° latitude, six months or more during each year have insufficient UV-B sunlight to produce optimal D levels. In far northern or southern locations, latitudes 45° and higher, even summer sun is too weak to provide optimum levels of vitamin D.13-15 A simple meter is available to determine UV-B levels where you live.
Vitamin D From Food

What the research on vitamin D tells us is that unless you are a fisherman, farmer, or otherwise outdoors and exposed regularly to sunlight, living in your ancestral latitude (more on this later), you are unlikely to obtain adequate amounts of vitamin D from the sun. Historically the balance of one's daily need was provided by food. Primitive peoples instinctively chose vitamin-D-rich foods including the intestines, organ meats, skin and fat from certain land animals, as well as shellfish, oily fish and insects. Many of these foods are unacceptable to the modern palate.

[...]

Vitamin D Miracles

Sunlight and vitamin D are critical to all life forms. Standard textbooks state that the principal function of vitamin D is to promote calcium absorption in the gut and calcium transfer across cell membranes, thus contributing to strong bones and a calm, contented nervous system. It is also well recognized that vitamin D aids in the absorption of magnesium, iron and zinc, as well as calcium.

Actually, vitamin D does not in itself promote healthy bone. Vitamin D controls the levels of calcium in the blood. If there is not enough calcium in the diet, then it will be drawn from the bone. High levels of vitamin D (from the diet or from sunlight) will actually demineralize bone if sufficient calcium is not present.

Vitamin D will also enhance the uptake of toxic metals like lead, cadmium, aluminum and strontium if calcium, magnesium and phosphorus are not present in adequate amounts.18 Vitamin D supplementation should never be suggested unless calcium intake is sufficient or supplemented at the same time.

Receptors for vitamin D are found in most of the cells in the body and research during the 1980s suggested that vitamin D contributed to a healthy immune system, promoted muscle strength, regulated the maturation process and contributed to hormone production.

During the last ten years, researchers have made a number of exciting discoveries about vitamin D. They have ascertained, for example, that vitamin D is an antioxidant that is a more effective antioxidant than vitamin E in reducing lipid peroxidation and increasing enzymes that protect against oxidation.19;20

Vitamin D deficiency decreases biosynthesis and release of insulin.21 Glucose intolerance has been inversely associated with the concentration of vitamin D in the blood. Thus, vitamin D may protect against both Type I and Type II diabetes.22

The risk of senile cataract is reduced in persons with optimal levels of D and carotenoids.23

PCOS (Polycystic Ovarian Syndrome) has been corrected by supplementation of D and calcium.24

Vitamin D plays a role in regulation of both the "infectious" immune system and the "inflammatory" immune system.25

Low vitamin D is associated with several autoimmune diseases including multiple sclerosis, Sjogren's Syndrome, rheumatoid arthritis, thyroiditis and Crohn's disease.26;27

Osteoporosis is strongly associated with low vitamin D. Postmenopausal women with osteoporosis respond favorably (and rapidly) to higher levels of D plus calcium and magnesium.28

D deficiency has been mistaken for fibromyalgia, chronic fatigue or peripheral neuropathy.1;28-30

Infertility is associated with low vitamin D.31 Vitamin D supports production of estrogen in men and women.32 PMS has been completely reversed by addition of calcium, magnesium and vitamin D.33 Menstrual migraine is associated with low levels of vitamin D and calcium.81

Breast, prostate, skin and colon cancer have a strong association with low levels of D and lack of sunlight.34-38

Activated vitamin D in the adrenal gland regulates tyrosine hydroxylase, the rate limiting enzyme necessary for the production of dopamine, epinephrine and norepinephrine. Low D may contribute to chronic fatigue and depression.39

Seasonal Affective Disorder has been treated successfully with vitamin D. In a recent study covering 30 days of treatment comparing vitamin D supplementation with two-hour daily use of light boxes, depression completely resolved in the D group but not in the light box group.40

High stress may increase the need for vitamin D or UV-B sunlight and calcium.41

People with Parkinsons and Alzheimers have been found to have lower levels of vitamin D.42;43

Low levels of D, and perhaps calcium, in a pregnant mother and later in the child may be the contributing cause of "crooked teeth" and myopia. When these conditions are found in succeeding generations it means the genetics require higher levels of one or both nutrients to optimize health.44-47

Behavior and learning disorders respond well to D and/or calcium combined with an adequate diet and trace minerals.48;49
Vitamin D and Heart Disease

Research suggests that low levels of vitamin D may contribute to or be a cause of syndrome X with associated hypertension, obesity, diabetes and heart disease.50 Vitamin D regulates vitamin-D-binding proteins and some calcium-binding proteins, which are responsible for carrying calcium to the "right location" and protecting cells from damage by free calcium.51 Thus, high dietary levels of calcium, when D is insufficient, may contribute to calcification of the arteries, joints, kidney and perhaps even the brain.52-54

Many researchers have postulated that vitamin D deficiency leads to the deposition of calcium in the arteries and hence atherosclerosis, noting that northern countries have higher levels of cardiovascular disease and that more heart attacks occur in winter months.55-56

Scottish researchers found that calcium levels in the hair inversely correlated with arterial calcium—the more calcium or plaque in the arteries, the less calcium in the hair. Ninety percent of men experiencing myocardial infarction had low hair calcium. When vitamin D was administered, the amount of calcium in the beard went up and this rise continued as long as vitamin D was consumed. Almost immediately after stopping supplementation, however, beard calcium fell to pre-supplement levels.27

Administration of dietary vitamin D or UV-B treatment has been shown to lower blood pressure, restore insulin sensitivity and lower cholesterol.58-60
The Battle of the Bulge

Did you ever wonder why some people can eat all they want and not get fat, while others are constantly battling extra pounds? The answer may have to do with vitamin D and calcium status. Sunlight, UV-B, and vitamin D normalize food intake and normalize blood sugar. Weight normalization is associated with higher levels of vitamin D and adequate calcium.61 Obesity is associated with vitamin-D deficiency.62-64 In fact, obese persons have impaired production of UV-B-stimulated D and impaired absorption of food source and supplemental D.65

Exercise Changes Brain

Exercise Changes Brain

HD Lighthouse Contributing Editor's Comment: Exercise is essential for preserving brain function for everyone. For some the loss of 'executive function' is the first symptom of HD. Here is another way exercise fights HD. Executive function is strongly preserved by exercise.

Older women (30+) seem to benefit the most from exercise. This may be because more women than men practice hormone replacement. Women that take replacement estrogen tend to exercise more. Some older men enjoy workouts that are boosted by testosterone.

Exercise Brain Benefits Confirmed for Humans
"The findings provide the first empirical confirmation of the relationship between cardiovascular fitness and neural degeneration as predicted in various academic studies on aging and cognition in both animal and human populations." Arthur Kramer, Ph.D., professor in the UIUC Department of Psychology, the Campus Neuroscience Program, and the Institute of Aviation; and a full-time faculty member in the Beckman Institute Human Perception and Performance Group. His fields of professional interest are perceptual organization and visual attention, acquisition and utilization of perceptual and cognitive skills, cognition and aging, and cognitive neuroscience.
Study is first to confirm link between exercise and changes in brain

CHAMPAIGN, Ill. -- Three key areas of the brain adversely affected by aging show the greatest benefit when a person stays physically fit. The proof, scientists say, is visible in the brain scans of 55 volunteers over age 55. The idea that fitness improves cognition in the aging is not new. Animal studies have found that aerobic exercise boosts cellular and molecular components of the brain, and exercise has improved problem-solving and other cognitive abilities in older people. A new study in the February issue of the Journal of Gerontology: Medical Sciences, however, is the first to show -- using high-resolution magnetic resonance imaging -- anatomical differences in gray and white matter between physically fit and less fit aging humans.

Gray matter consists of thin layers of tissue of cell bodies such as neurons and support cells that are critically involved in learning and memory. White matter is the myelin sheath containing the nerve fibers that transmit signals throughout the brain.

"As people age, especially after age 30, these tissues shrink in a pattern closely matched by declines in cognitive performance." Kramer said. "We found differences in three areas of the brain, the frontal, temporal and parietal cortexes. There were very distinct differences particularly in two types of tissue, the gray matter and white matter. Nobody has reported this before."

[...]

"Interestingly, we found that fitness per se didn't have any influence on brain density," said Kramer, a professor of psychology and member of the Beckman Institute for Advanced Science and Technology at Illinois. "It is fitness as it interacts with age that has the positive effects. Older adults show a real decline in brain density in white and gray areas, but fitness actually slows that decline."

[...]

"This, to our knowledge, is the first human data providing a potential anatomical account of the cognitive effects that we and others have found over the years," Kramer said. "Our data also suggest that more research is clearly needed to actually do a thorough examination of brain structure and functioning, and the impact of interventions such as fitness and cognitive training."

In 1999, Kramer and colleagues reported in the journal Nature that previously sedentary people over age 60 who walked rapidly for 45 minutes three days a week can significantly improve mental-processing abilities that decline with age, and particularly tasks that rely heavily on the frontal lobes of the brain.

For their meta-analysis paper, researchers reviewed 18 intervention studies done between 1966 and 2001 and involving hundreds of participants ages 55 and older. Fitness training was found to show "robust but selective benefits for cognition, with the largest fitness-induced benefits occurring for executive-control processes."

[...]

Other main conclusions from the meta-analysis: Exercise programs involving both aerobic exercise and strength training produced better results on cognitive abilities than either one alone.

Older adults benefit more than younger adults do, possibly, Kramer said, because older adults have more to gain as age-related declines become more prevalent.

More than 30 minutes of exercise per session produce the greatest benefit, a finding consistent with many existing guidelines for adults. The studies were funded by the National Institute on Aging (National Institutes of Health) and the New York-based Institute for the Study of Aging.

Exercise and BDNF HDLighthouse.org

HDLighthouse.org

Conclusion
Exercise is a simple and widely practised behavior that activates molecular and cellular cascades that support and maintain brain plasticity. It induces expression of genes associated with plasticity, such as that encoding BDNF, and in addition promotes brain vascularization, neurogenesis, functional changes in neuronal structure and neuronal resistance to injury. Significantly, these effects occur in the hippocampus, a brain region central to learning and memory. BDNF availability could be crucial for these mechanisms. Exercise-driven increases in the level of hippocampal BDNF are controlled by neuronal activity, neurotransmitters and interactions with peripheral factors that include estrogen, corticosterone and possibly IGF-1. The peripheral influence illustrates how exercise can relate overall body status to brain function. Exercise recruits use-dependent plasticity mechanisms that prepare the brain to encode meaningful information from the environment and, at the same time, activates mechanisms that protect the brain from damage. By inducing BDNF and other molecules, exercise strengthens neuronal structure and facilitates synaptic transmission, thus, priming activated cells for encoding.

The clinical literature has recognized for years that exercise affects overall health and brain function. Scientific studies are now strengthening the premise that exercise can benefit brain function and are encouraging additional clinical research in this area.

Exercise: a behavioral intervention to enhance brain health

Exercise: a behavioral intervention to enhance bra...[Trends Neurosci. 2002] - PubMed Result

Exercise: a behavioral intervention to enhance brain health and plasticity.

Cotman CW, Berchtold NC.

Institute for Brain Aging and Dementia, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-4540, USA. cwcotman@uci.edu

Extensive research on humans suggests that exercise could have benefits for overall health and cognitive function, particularly in later life. Recent studies using animal models have been directed towards understanding the neurobiological bases of these benefits. It is now clear that voluntary exercise can increase levels of brain-derived neurotrophic factor (BDNF) and other growth factors, stimulate neurogenesis, increase resistance to brain insult and improve learning and mental performance. Recently, high-density oligonucleotide microarray analysis has demonstrated that, in addition to increasing levels of BDNF, exercise mobilizes gene expression profiles that would be predicted to benefit brain plasticity processes. Thus, exercise could provide a simple means to maintain brain function and promote brain plasticity.

Nutrition and schizophrenia: beyond omega-3 fatty ...[Prostaglandins Leukot Essent Fatty Acids. 2004] - PubMed Result

Nutrition and schizophrenia: beyond omega-3 fatty ...[Prostaglandins Leukot Essent Fatty Acids. 2004] - PubMed Result

Nutrition and schizophrenia: beyond omega-3 fatty acids.

Peet M.

Swallownest Court Hospital, Aughton Road, Sheffield S26 4th, UK. malcolmpeet@Yahoo.com

There are now five placebo-controlled trials of EPA in the treatment in schizophrenia, and four of these have given positive or partly positive findings. A cross-national ecological analysis of international variations in outcome of schizophrenia in relation to national dietary practices, showed that high consumption of sugar and of saturated fat is associated with a worse long-term outcome of schizophrenia. It is known that a high sugar, high fat diet leads to reduced brain expression of brain-derived neurotrophic factor (BDNF) which is responsible for maintaining the outgrowth of dendrites. Low brain BDNF levels also lead to insulin resistance which occurs in schizophrenia and is associated with diseases of the metabolic syndrome. It appears that the same dietary factors which are associated with the metabolic syndrome, including high saturated fat, high glycaemic load, and low omega-3 PUFA, may also be detrimental to the symptoms of schizophrenia, possibly through a common mechanism involving BDNF.

Diet, diabetes and schizophrenia: review and hypothesis -- Peet 184 (47): s102 -- The British Journal of Psychiatry

Diet, diabetes and schizophrenia: review and hypothesis -- Peet 184 (47): s102 -- The British Journal of Psychiatry

There is substantial evidence that schizophrenia is associated with abnormalities of phospholipid metabolism and cell membrane PUFA levels (Peet, 2002). Two studies have shown that levels of PUFA in the normal daily diet correlate with the severity of schizophrenia symptoms. Mellor et al (1996) showed significant negative correlations between dietary intake of omega-3 fatty acids and symptoms of schizophrenia and of tardive dyskinesia. In a separate study, Stokes (2003) found that total PUFA in the normal daily diet correlated negatively with severity of schizophrenia symptoms and that this was independent of the dietary intake of other nutrients.

In summary, people with schizophrenia consume the type of diet that is known to promote diseases of the metabolic syndrome (i.e. high in saturated fat, low in fibre, with a high glycaemic load). Furthermore, there is emerging evidence of an association between dietary factors and the severity and long-term outcome of schizophrenia.

[...]

Diet, diabetes and schizophrenia: a hypothesis
Insulin resistance results from an interplay of genetic and lifestyle factors (Ukkola & Bouchard, 2001). Insulin resistance is not in itself necessarily harmful and indeed may confer an evolutionary advantage (Colagiuri & Miller, 2002). Australian aboriginals show evidence of increased insulin resistance but this does not manifest itself as pathological until they give up their traditional lifestyle and adopt Western dietary practices (O’Dea, 1991). People with schizophrenia who exhibit insulin resistance at the start of their illness will therefore have an increased susceptibility to the adverse effects of a poor diet.

The most parsimonious explanation for the increased prevalence of diabetes in patients with schizophrenia is that a genetic predisposition to insulin resistance is compounded by an unhealthy lifestyle and the effect of antipsychotic medication on food intake. The genetic influence is suggested by the increased frequency of diabetes in the relatives of patients with schizophrenia (Mukherjee et al, 1989). However, evidence of a significant association between diet and the outcome and severity of schizophrenia raises the possibility that both diabetes and schizophrenia share a common pathology which is influenced by lifestyle factors such as diet and exercise. One physiological factor that could partly explain the link between diabetes, schizophrenia and diet is brain-derived neurotrophic factor (BDNF). This protein is required to maintain dendrites (Gorski et al, 2003), and its expression in the prefrontal cortex shows a significant increase during young adulthood at a time when the frontal cortex matures both structurally and functionally (Webster et al, 2002). The peak requirement for BDNF to preserve dendritic outgrowth thus occurs at the time of life when schizophrenia has its peak age of onset. Apart from influences on neuronal architecture, BDNF is also a neurotransmitter modulator and facilitates long-term potentiation in the hippocampus (Lessman et al, 2003). It has recently been shown that BDNF expression is reduced in the prefrontal cortex of patients with schizophrenia, and it was suggested that this might be a central component of the disease process (Weickert et al, 2003). Polymorphism of the BDNF gene has been associated with the susceptibility to schizophrenia (Szekeres et al, 2003) and with clozapine responders (Hong et al, 2003). It is known that brain expression of BDNF is reduced by a high-fat, high-sugar diet (Molteni et al, 2002) and increased by exercise (Cotman & Berchtold, 2002). In BDNF knockout mice, neuronal soma size and dendrite density in the prefrontal cortex are reduced (Gorski et al, 2003), and the same structural abnormalities have been reported in the brains of people with schizophrenia (Broadbelt et al, 2002). Brain-derived neurotrophic factor is also involved in the control of insulin resistance. Heterozygous BDNF knockout mice show a 50% reduction in brain levels of BDNF, and they also show hyperphagia and features of the metabolic syndrome (Duan et al, 2003). Administration of BDNF into the cerebral ventricles of obese/diabetic rodent models reduces obesity and improves glucose tolerance (Nakagawa et al, 2000), suggesting that the effect of BDNF on the metabolic syndrome is centrally mediated.

On the basis of the findings discussed so far, it is possible to construct a hypothesis whereby the high-fat, high-sugar diet of patients with schizophrenia leads to reduced expression of BDNF in the brain. This would exacerbate any genetically determined abnormalities of BDNF expression. Although very speculative, this provides a possible explanatory model for the observed epidemiological association between a high-fat, high-sugar diet and poor long-term outcome of schizophrenia. Such a diet would also lead to an increased risk of diabetes, through both peripheral and central mechanisms.

There is evidence that typical and atypical antipsychotic medications have differential effects upon BDNF. Haloperidol has been found to reduce hippocampal expression of BDNF, whereas BDNF expression is increased by olanzapine and clozapine (Bai et al, 2003). However, since there is no clear correlation between these effects and the efficacy and side-effect profiles of these drugs, at least in the short term, it is unlikely that these agents are acting through an effect on BDNF.

[...]

DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHOD
RESULTS
DISCUSSION
Clinical Implications and...
REFERENCES


Clinical importance of lifestyle interventions in schizophrenia
In order to reduce the risk of obesity, diabetes and coronary heart disease in people with schizophrenia, the importance of a healthy lifestyle – including good dietary practices and sufficient exercise – cannot be overemphasised. Because insulin resistance is a feature associated with schizophrenia independently of any specific drug treatment, lifestyle advice should be given to all patients with a diagnosis of schizophrenia. This should start immediately as part of the package of care at the first onset of illness.

The evidence presented allows the hypothesis that a diet low in saturated fat, high in polyunsaturated fatty acids and low in glycaemic load might be beneficial also in alleviating the symptoms of schizophrenia. There are five placebo-controlled trials of omega-3 fatty acids in the treatment of schizophrenia, of which three showed significant benefit, one showed benefit of omega-3 fatty acids only in a subgroup of patients already receiving treatment with clozapine, and one showed no advantage of omega-3 fatty acids over placebo (Peet, 2004). The proposition that the symptoms and the outcome of schizophrenia might be improved by a diet low in saturated fat and low in sugar has not been systematically investigated, although there are anecdotal reports of the successful use of this approach (Meiers, 1973).

Know Your Fats: Gamma-Linolenic Acid

Know Your Fats: Gamma-Linolenic Acid

The human body uses fatty acids from food for building tissues and for specialized functions such as the production of prostaglandins, localized tissue hormones. One major group of fatty acids is called essential fatty acids, which are polyunsaturated, and include two major groups, omega-3 and omega-6 fatty acids. They are called "essential" because the body cannot make them but must get them from food.

[...]

GLA is found in small amounts in organ meats and in certain seed oils such as evening primrose oil, borage oil, and black currant oil. Hemp oil also contains GLA but this oil has no history of consumption by humans. The percentages of GLA in these specialty oils are as follows:

Evening Primrose Oil 10%
Black Currant Oil 17%
Borage Oil 23%

These three oils are available in capsule form. The body needs an enzyme called delta-6 desaturase (D6D) to transform linoleic acid into GLA. Under normal conditions, most people make adequate amounts of D6D and hence the by-product GLA; however, a number of disease and deficiency conditions as well as components of the modern diet can interfere with the conversion of linoleic acid to GLA. Diabetics, for example, do not normally make adequate amounts of D6D and hence of GLA, nor do people with poor pituitary or thyroid function. Both malnutrition and overeating can interfere with D6D and inhibit the production of GLA. Trans fatty acids definitely inhibit the production of GLA as does overconsumption of sugar and alcohol. Deficiencies of protein, zinc, biotin and vitamins B6, B12 and E can all inhibit D6D function and hence the production of GLA. In addition, some individuals are not genetically programed to produce D6D at all, mainly those whose ancestors had lots of preformed D6D metabolites from organ meats and fish in their diets. Researchers have called such individuals "obligate carnivores." They are especially prone to diseases like diabetes and alcoholism if they do not eat enough fish and organ meat.

Some of the disease conditions that result from defective D6D function include premature aging, irritable bowel syndrome, cirrhosis of the liver, skin conditions like eczema, menstrual problem such as PMS, noncancerous breast disease, Sjogren’s syndrome, alcoholism, diabetes and cancer. Thus, investigators have hypothesized that GLA can be an important component of treatment for these conditions.

[...]

Other studies have shown that GLA has a favorable effect on cardiovascular risk factors, notably a reduction in the size of plaque in vessel walls.

The review article also notes that GLA is unique among the omega-6 family in its "potential to suppress tumor growth and metastasis." Other studies report very favorable results in the treatment of diabetic neuropathy with GLA.

Several studies involving rats have indicated that GLA can have a favorable effect on blood pressure and one human study, carried out in France ,found the GLA not only lowered blood pressure but had a favorable effect on other cardiovascular risk factors (Bratisl Led Listy 2002;103(3):101-7).

Studies that looked at the effect of GLA on skin conditions have been mixed, some showing no effect but others resulting in the alleviation of symptoms of dermatitis, especially in young children.

Finally, GLA has been shown to encourage weight loss in individuals who are considerably overweight, making it a good aid for dieting (Horrobin DF, ed. Clinical Uses of Essential Fatty Acids. Montreal: Eden Press, pp 53-61, 1982).

Eat your liver!

Subjective Experiences During Dopamine Depletion -- de HAAN et al. 162 (9): 1755 -- Am J Psychiatry

Subjective Experiences During Dopamine Depletion -- de HAAN et al. 162 (9): 1755 -- Am J Psychiatry

To the Editor: A paradigm that induces acute dopamine depletion with the drug alphamethylpara tyrosine (AMPT), a reversible inhibitor of tyrosine hydroxylase, has been used successfully to assess the occupancy of striatal dopamine D2 receptors by endogenous dopamine in vivo (1). Here we describe the dramatic subjective experiences induced by acute dopamine depletion in one healthy volunteer. They included a whole spectrum of psychiatric symptoms and highlighted the contribution of the dopaminergic system to diverse major psychiatric disorders.

In our study, dopamine depletion was achieved by oral administration of 4.5 g AMPT in 25 hours, as described earlier (1). Striatal D2 receptors were assessed at baseline and after acute dopamine depletion by using the bolus/constant infusion [123I]IBZM technique (1). Acquisition, reconstruction, and analysis of the single photon emission computed tomography data were performed as described previously (2).

Mr. A was a healthy, extraverted, very well functioning 21-year-old medical student without even minor psychological difficulties or psychiatric disorders in his family. His Global Assessment of Functioning Scale score was 97. Written informed consent was obtained from Mr. A. We will describe the spontaneous reported subjective experiences after he started the first dose of 750 mg AMPT at t=0 hours (1).

After 7 hours, Mr. A felt more distance between himself and his environment. Stimuli had less impact; visual and audible stimuli were less sharp. He experienced a loss of motivation and tiredness. After 18 hours, he had difficulty waking up and increasing tiredness; environmental stimuli seemed dull. He had less fluency of speech. After 20 hours, he felt confused. He felt tense before his appointment and had an urge to check his watch in an obsessive way.

After 24 hours, Mr. A had inner restlessness, flight of ideas; his ideas seemed inflicted, and he could not remember them. He felt a loss of control over his ideas. After 28 hours, he felt ashamed, frightened, anxious, and depressed. He was afraid that the situation would continue. At that time, blepharospasm, mask face, and tremor were noted. After 30 hours, he was tired and slept 11 hours. After 42 hours, he had poor concentration. In the next hours, he returned to normal.

The striatal-to-nonspecific binding ratio was 27% higher after Mr. A took AMPT compared to the baseline situation, indicating severe acute dopamine depletion (1).


During increasing dopamine depletion in this case, a range of subjective experiences appeared and disappeared consecutively. These experiences resembled negative symptoms, obsessive-compulsive symptoms, thought disorders, and anxiety and depressive symptoms and highlight the importance of the role of dopamine in major psychiatric disorders. In former studies, AMPT was found to lower mood, induce fatigue, decrease subjective alertness, and/or induce extrapyramidal symptoms in some healthy individuals (reviewed in reference 3).

Emotion-based decision-making in healthy subjects: short-term effects of reducing dopamine levels

SpringerLink - Journal Article

Emotion-based decision-making in healthy subjects: short-term effects of reducing dopamine levels


Abstract
Introduction

Converging evidences from animal and human studies suggest that addiction is associated with dopaminergic dysfunction in brain reward circuits. So far, it is unclear what aspects of addictive behaviors are related to a dopaminergic dysfunction.
Discussion We hypothesize that a decrease in dopaminergic activity impairs emotion-based decision-making.

[...]

Our results suggest a direct link between a reduced dopaminergic activity and poor emotion-based decision-making characterized by shortsightedness, and thus difficulties resisting short-term reward, despite long-term negative consequences. These findings have implications for behavioral and pharmacological interventions targeting impaired emotion-based decision-making in addictive disorders.

Huge new study: Vitamin D cuts cancer by 60%- get out in the SUN!

globeandmail.com: Health

Sweeping cancer edict: take vitamin D daily

MARTIN MITTELSTAEDT

From Friday's Globe and Mail
TORONTO — The Canadian Cancer Society plans to announce Friday that all adults should start taking vitamin D, coinciding with the release of a groundbreaking U.S. study indicating the supplement cuts the risk of cancer by an astounding 60 per cent. The move is believed to be the first time a major public-health organization has endorsed daily use of the sunshine vitamin as a cancer-prevention therapy for an entire population.

Sunday, June 24, 2007

Getting a good night's sleep can mean waking early

Living Well: Getting a good night's sleep can mean waking early

Like many of us, Martha Lentz looks forward to weekends, especially the three-day variety. She gets a chance to sleep in.

"I know better," says Lentz, laughing. "But I do it anyway. I enjoy it."

What Lentz knows better is how to get a good night's sleep. She is a research associate professor at the University of Washington's School of Nursing who has specialized in sleep patterns and circadian rhythms since the early 1980s.

A consistent wakeup time tops the Get More and Better Sleep list. Even if it means actually getting less sleep on a weekend, when everyone with a sociable bone in their bodies stays up later than normal.

"The research is clear that waking up at the same time exposes your body to similar amounts of light each day, which in turn synchronizes your circadian rhythms," said Lentz, a Ph.D. who has performed sleep and aging studies as part of UW's Center for Women's Health Research.

Lentz said properly tuned circadian rhythms in your body leads to feeling more refreshed and alert during the day and, appropriately, more drowsy at bedtime. Getting enough light earlier in the day is what makes the difference. It's not the simple act of waking up at the same time forcing you to get to bed earlier, though a regular bedtime only improves your circadian cycle.

"People ask me all the time about what's the best thing to do for better sleep," said James M. Krueger, professor of neurobiology at Washington State University and a noted sleep researcher who is pioneering new studies on whether regions of the brain are 'asleep' while a person is awake. "I tell them be as regular as you can about both getting to sleep and waking up."

Dunning-Kruger effect - Wikipedia, the free encyclopedia

Dunning-Kruger effect - Wikipedia, the free encyclopedia

Dunning-Kruger effect
From Wikipedia, the free encyclopedia
(Redirected from Dunning-Kruger Syndrome)

The Dunning-Kruger effect is the phenomenon whereby people who have little knowledge systematically think that they know more than others who have much more knowledge.

The phenomenon was demonstrated in a series of experiments performed by Justin Kruger and David Dunning, then both of Cornell University. Their results were published in the Journal of Personality and Social Psychology in December 1999.[1]

Kruger and Dunning noted a number of previous studies which tend to suggest that in skills as diverse as reading comprehension, operating a motor vehicle, and playing chess or tennis, that "ignorance more frequently begets confidence than does knowledge"[1] (as Charles Darwin put it). They hypothesized that with a typical skill which humans may possess in greater or lesser degree,
incompetent individuals tend to overestimate their own level of skill,
incompetent individuals fail to recognize genuine skill in others,
incompetent individuals fail to recognize the extremity of their inadequacy,
if they can be trained to substantially improve their own skill level, these individuals can recognize and acknowledge their own previous lack of skill.

They set out to test these hypotheses on human subjects consisting of Cornell undergraduates who were registered in various psychology courses.

In a series of studies, Kruger and Dunning examined self-assessment of logical reasoning skills, grammatical skills and humor. After being shown their test score, the subjects were again asked to estimate their own rank whereupon the competent group accurately estimated their rank, while the incompetent group still overestimated their own rank. As Dunning and Kruger noted,“ Across 4 studies, the authors found that participants scoring in the bottom quartile on tests of humor, grammar, and logic grossly overestimated their test performance and ability. Although test scores put them in the 12th percentile, they estimated themselves to be in the 62nd. ”


Meanwhile, people with true knowledge tended to underestimate their competence.

A followup study suggests that grossly incompetent students improve both their skill level and their ability to estimate their class rank only after extensive tutoring in the skills they had previously lacked.

Daniel Ames and Lara Kammrath extended this work to sensitivity to others, and the subjects' perception of how sensitive they were.[2]

Some more work by Burson Larrick and Joshua Klayman[3] has suggested that the effect is not so obvious and may be due to noise and bias levels.

Dunning and Kruger won the 2000 Ig Nobel prize for their work.[4]

Infant Feeding Practices and Their Possible Relationship to the Etiology of Diabetes Mellitus -- Work Group on Cow's Milk Protein and Diabetes Mellitus 94 (5): 752 -- Pediatrics

Infant Feeding Practices and Their Possible Relationship to the Etiology of Diabetes Mellitus -- Work Group on Cow's Milk Protein and Diabetes Mellitus 94 (5): 752 -- Pediatrics

Infant Feeding Practices and Their Possible Relationship to the Etiology of Diabetes Mellitus
Work Group on Cow's Milk Protein and Diabetes Mellitus


1. Insulin-dependent diabetes mellitus develops within a group of individuals who carry specific diabetes susceptibility traits. Because all of the potential diabetes "susceptibility genes" are not known, currently it is not possible to identify all individuals at risk. It appears, however, that a small percentage of such individuals will ever develop clinical diabetes mellitus.

2. The autoimmune destructive process may be triggered by a number of environmental events.

3. Early exposure of infants to cow's milk protein may be an important factor in the initiation of the cell destructive process in some individuals. It is not known whether the cow's milk protein in commercially available infant formulas is associated with this process.

4. The avoidance of cow's milk protein for the first several months of life may reduce the later development of IDDM or delay its onset in susceptible individuals.

5. Research directed toward further defining the possible relationship between infant feeding practices and the development of IDDM is needed.

Saturday, June 23, 2007

Meditation May Sharpen Attention Skills, Study Shows Meditation Appears To Train The Brain To Pay Closer Attention - CBS News

Meditation May Sharpen Attention Skills, Study Shows Meditation Appears To Train The Brain To Pay Closer Attention - CBS News

Meditation may train the brain to pay close attention, a new study shows.

The study comes from researchers including Richard Davidson, PhD, professor of psychology and psychiatry at the University of Wisconsin in Madison.

They studied 17 people who were experienced in meditation and 23 people of similar backgrounds who were novices in meditation.

[...]

At the end of their meditation training, the researchers tested participants' attention skills.

In the attention test, participants watched a series of letters shown one by one on a computer screen. Each letter was displayed for less than a second.

Every now and then, a letter was followed by a number, instead of another letter. Participants were asked to name the numbers, which (like the letters) only appeared for a split second.

The researchers didn't ask participants to meditate during the tests.

Compared with the meditation novices, participants who had attended the three-month intensive meditation retreat were better at noticing the numbers mixed into the string of letters. The researchers say the findings show that meditation served as mental training that improved control over attention.

A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning

ScienceDirect - Neuroscience : A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning

Abstract

We have investigated a potential mechanism by which a diet, similar in composition to the typical diet of most industrialized western societies rich in saturated fat and refined sugar (HFS), can influence brain structure and function via regulation of neurotrophins. We show that animals that learn a spatial memory task faster have more brain-derived neurotrophic factor (BDNF) mRNA and protein in the hippocampus. Two months on the HFS diet were sufficient to reduce hippocampal level of BDNF and spatial learning performance. Consequent to the action of BDNF on synaptic function, downstream effectors for the action of BDNF on synaptic plasticity were reduced proportionally to BDNF levels, in the hippocampus of rats maintained on the HFS diet between 2 and 24 months. In particular, animals maintained on the HFS diet showed a decrease in levels of: (i) synapsin I mRNA and protein (total and phosphorylated), important for neurotransmitter release; (ii) cyclic AMP-response element-binding protein (CREB) mRNA and protein (total and phosphorylated); CREB is required for various forms of memory and is under regulatory control of BDNF; (iii) growth-associated protein 43 mRNA, important for neurite outgrowth, neurotransmitter release, and learning and memory. Diet-related changes were specific for the hippocampus consequent to its role in memory formation, and did not involve neurotrophin-3, another member of the neurotrophin family.

Our results indicate that a popularly consumed diet can influence crucial aspects of neuronal and behavioral plasticity associated with the function of BDNF.

Diet, diabetes and schizophrenia: review and hypothesis -- Peet 184 (47): s102 -- The British Journal of Psychiatry

Diet, diabetes and schizophrenia: review and hypothesis -- Peet 184 (47): s102 -- The British Journal of Psychiatry

However, evidence of a significant association between diet and the outcome and severity of schizophrenia raises the possibility that both diabetes and schizophrenia share a common pathology which is influenced by lifestyle factors such as diet and exercise. One physiological factor that could partly explain the link between diabetes, schizophrenia and diet is brain-derived neurotrophic factor (BDNF). This protein is required to maintain dendrites (Gorski et al, 2003), and its expression in the prefrontal cortex shows a significant increase during young adulthood at a time when the frontal cortex matures both structurally and functionally (Webster et al, 2002). The peak requirement for BDNF to preserve dendritic outgrowth thus occurs at the time of life when schizophrenia has its peak age of onset. Apart from influences on neuronal architecture, BDNF is also a neurotransmitter modulator and facilitates long-term potentiation in the hippocampus (Lessman et al, 2003). It has recently been shown that BDNF expression is reduced in the prefrontal cortex of patients with schizophrenia, and it was suggested that this might be a central component of the disease process (Weickert et al, 2003). Polymorphism of the BDNF gene has been associated with the susceptibility to schizophrenia (Szekeres et al, 2003) and with clozapine responders (Hong et al, 2003). It is known that brain expression of BDNF is reduced by a high-fat, high-sugar diet (Molteni et al, 2002) and increased by exercise (Cotman & Berchtold, 2002). In BDNF knockout mice, neuronal soma size and dendrite density in the prefrontal cortex are reduced (Gorski et al, 2003), and the same structural abnormalities have been reported in the brains of people with schizophrenia (Broadbelt et al, 2002). Brain-derived neurotrophic factor is also involved in the control of insulin resistance. Heterozygous BDNF knockout mice show a 50% reduction in brain levels of BDNF, and they also show hyperphagia and features of the metabolic syndrome (Duan et al, 2003). Administration of BDNF into the cerebral ventricles of obese/diabetic rodent models reduces obesity and improves glucose tolerance (Nakagawa et al, 2000), suggesting that the effect of BDNF on the metabolic syndrome is centrally mediated.

On the basis of the findings discussed so far, it is possible to construct a hypothesis whereby the high-fat, high-sugar diet of patients with schizophrenia leads to reduced expression of BDNF in the brain. This would exacerbate any genetically determined abnormalities of BDNF expression. Although very speculative, this provides a possible explanatory model for the observed epidemiological association between a high-fat, high-sugar diet and poor long-term outcome of schizophrenia. Such a diet would also lead to an increased risk of diabetes, through both peripheral and central mechanisms

Cameron's bag raises a few eyebrows

Cameron's bag raises a few eyebrows

Actress Cameron Diaz appears to have committed a major fashion crime in Peru.

The voice of Princess Fiona in the animated Shrek films may have inadvertently offended Peruvians.

They suffered decades of violence from a Maoist guerrilla insurgency by touring there on Friday with a bag emblazoned with one of Mao Zedong's favourite political slogans.

While she explored the Inca city of Machu Picchu high in Peru's Andes, Diaz wore over her shoulder an olive green messenger bag emblazoned with a red star and the words 'Serve the People' printed in Chinese on the flap, perhaps Chinese Communist leader Mao's most famous political slogan.

While the bags are marketed as trendy fashion accessories in some world capitals, the phrase has particular resonance in Peru.

The Maoist Shining Path insurgency took Peru to the edge of chaos in the 1980s and early 1990s with a campaign of massacres, assassinations and bombings.

Nearly 70,000 people were killed during the insurgency.

A prominent Peruvian human rights activist said the star of There's Something About Mary should have been a little more aware of local sensitivities when picking her accessories.

"It alludes to a concept that did so much damage to Peru, that brought about so many victims," said Pablo Rojas about the bag's slogan.

"I don't think she should have used that bag where the followers of that ideology" did so much damage.

Case report: The combined use of amantadine and l-dopa/ carbidopa in the treatment of chronic brain injury - Brain Injury

Case report: The combined use of amantadine and l-dopa/ carbidopa in the treatment of chronic brain injury - Brain Injury

Abstract
The frontal lobes are particularly vulnerable to injury during trauma. The syndrome commonly attributed to frontal lobe dysfunction includes problems with impulsivity, perseveration, disinhibition, amotivation, attention, planning, and problem solving. These symptoms can respond to certain phar macologic interventions, such as the dopaminergic agents. The case of a 50 year old woman who showed persistent frontal dysfunction 5 years post injury is described. After treatment with amantadine alone, she showed decreased impulsivity and perseveration and improved executive function. Further positive response was obtained with the addition of l dopa carbidopa, with additional improvements in constructional praxis, divided auditory attention, and cognitive flexibility. Her improved function ing following treatment demonstrates the potential for increasing effectiveness through a combination of dopaminergic agents. No side effects were observed, and the patient maintained gains at follow up. The rationale for using dopaminergic agents alone and in combination is discussed.

This drug, Amantadine, appears to be an anti-viral drug used to treat frontal lobe dysfunction, as in ADD. I want to find out more about it.

Friday, June 22, 2007

Scientists discover diabetes link to Parkinson's

Scotsman.com News - Health - Scientists discover diabetes link to Parkinson's

A TEAM of scientists has discovered that keeping fit and staying clear of diabetes could help ward off Parkinson's disease.

Heriot-Watt University staff have found a mechanism linking the development of Parkinson's to people who have Type II diabetes.


Professor James Timmons, professor of Exercise Biology at the School of Life Sciences, led the team, which discovered that the biochemical changes brought about by diabetes switch off a gene called the PINK1 gene, and loss of function of this gene is an established cause of Parkinson's.

The team compared 200 tissue samples donated by volunteers, many of whom had been diagnosed with Type II diabetes.

Prof Timmons explained: "The loss of PINK1 is not the only cause of Parkinson's, but discovering this direct link between diabetes and the regulation of the PINK1 gene is the first example of a molecular mechanism potentially linking the two terrible illnesses, rather than just a statistical association drawn from population studies."

Again, I'm looking for the dopamine, or other psiological link, between insulin resistance/obesity and ADD.

Scientists unveil the brain's CEO-Mumbai-Cities-The Times of India

Scientists unveil the brain's CEO-Mumbai-Cities-The Times of India

MUMBAI: Why do some people who are truly smart and talented still struggle and flail through life like headless chickens?

Why do they act as though they lack the rudimentary ability to plan and organise their time and space, to initiate and execute projects to fruition?

And, like monkeys tearing down banana blossoms in favour of more substantive but late-arriving bonanzas, why do such people also have such a hard time resisting the temptation of more immediate gratifications?

Recent research suggests that rather than being wilful or perverse, many of these puzzling underachievers may actually be suffering from neurological abnormalities involving the brain's CEO - a control centre that is really an array of executive functions that orchestrate resources such as memory, language and attention to achieve a goal, be it a fraction of a second or five years from now.

Executive functions enable you to hold on to a mental image of destination.

A deficiency in this crucial area could make the person "future-blind", researchers say.

This was dramatically highlighted in the celebrated case of Phineas Gage, an upwardly railroad contractor, otherwise a Victorian model of rectitude and diligence who turned into an aimless drifter and cussed sociopath after surviving grievous brain injury in a freak accident.

Noted neurologist Antonio Damasio examined Gage's case in ‘Descartes Error', his best-selling synthesis of emotion and reason.

He and his wife Hanna have studied patients with similar front-lobe damage that similarly devastating impact which leaves IQ, memory and language intact but with a profound lack of feeling and an inability to put current events in context and make judgments about the future.

Leading to a short term orientation. Short term pleasures over longer term investments. Also, minor events have a much larger emotional impact than you would guess, but dissapate quickly as well. So something bad happens, and you are thrown into misery. The next day you feel fine again, whereas traditional depression lingers for months and months.

Depression and vascular disease: what is the relat...[J Affect Disord. 2004] - PubMed Result

Depression and vascular disease: what is the relat...[J Affect Disord. 2004] - PubMed Result

Depression and vascular disease: what is the relationship?

Thomas AJ, Kalaria RN, O'Brien JT.

Wolfson Research Centre, Department of Psychiatry and Institute for Ageing and Health, University of Newcastle upon Tyne, Newcastle upon Tyne NE4 6BE, UK. a.j.thomas@ncl.ac.uk

BACKGROUND: the 'vascular depression' hypothesis proposes that vascular disease predisposes to, precipitates or perpetuates depression, and this proposal has stimulated further research into the relationship of depression to vascular disease. METHODS: We investigated the nature of the relationship between depression and vascular diseases by reviewing epidemiological, clinical, neuroimaging and neuropathology studies which have reported on the relationship of depression to coronary artery disease, stroke disease, alterations in blood pressure, vascular dementia, diabetes mellitus and cholesterol levels and by reviewing potential mechanisms by which depression could be associated with vascular diseases. RESULTS: there is abundant and increasing evidence from these different lines of research that depression has a bidirectional association with vascular diseases and plausible mechanisms exist which explain how depression might increase these vascular diseases and vice versa. LIMITATIONS: this was not a systematic review and so not every report of relevance has been included. CONCLUSIONS: depression has a clear bidirectional relationship with vascular diseases. Further study is needed to clarify the mechanisms involved and to investigate the benefits of conventional and novel treatments for vascular diseases in depressive illness.

Thursday, June 21, 2007

8 Practical Tips to Cure Your Internet ADD (Attention Deficit Disorder) | zen habits

8 Practical Tips to Cure Your Internet ADD (Attention Deficit Disorder) | zen habits

8 Practical Tips to Cure Your Internet ADD (Attention Deficit Disorder)

This is a guest post from Alex Brie of Hack the Day.

You know you have it - every nerd does - the tickling sensation in the left hand to press Alt+Tab or Cmd+Tab to switch apps, Internet browser tabs or windows, to go from your email to Firefox, Instant Messenger, Twitter, your current work and back to Firefox.

No matter what you do, it seems like nothing is important enough to prevent you from writing a brief IM message to your best bud about what the latest joke your office mates have just sent you by email.

Nothing is too important that can’t wait till after you play a quick online flash game or read another blog post while your boss is out of the room.

Internet Attention Deficit Disorder is the productivity killer affecting most office workers today - the stringent urge to “browse just a little more” in between your daily work tasks; to peek at the Digg homepage, check out the hottest YouTube video of the day, skim through your blog feeds reading what happened in the last hour, to jump eagerly whenever Outlook or Mail.app alert you of new mail and interrupt all activity when you get via IM a link to a funny picture.

Sure, GTD, Zen To Done and most other productivity methods try to help you manage your priorities better and ignore the insignificant. But how could you ever do this if there’s always “one more” blog post to read, “one more” IM to answer, “one more” twitter status to check out?

Enter our brief list of tips to detect, manage, contain and even cure the Internet ADD. Here on Zen Habits you’ve read plenty of tips on how to focus on the most important tasks of the day and ignore the trivial things. But now we’ll look at tips to do that, aimed specifically at the Internet ADD:

Attention Deficit Hyperactive Disorder and the Benefits of Nature

Troubled Teens Resources - Attention Deficit Hyperactive Disorder and the Benefits of Nature

Attention deficit hyperactive disorder has recently been viewed as amenable to treatment that simply involves getting teenagers outside, away from iPods,video games,TV,and all the sedentary ways that accompany those habits. Though we mostly hear from health specialists from the American perspective, doctors in England are making similar studies.

“For too long we have seriously underestimated the benefits nature has for the health of our nation. Everyone, from government to charities like the RSPB to private landowners, needs to work together to give people more access to nature.”

Parents who are considering enrolling their teen in a troubled teen boarding school might want to consider the lay of the land around it. Is it located where the beauty of nature can be one of the healing elements in your troubled teen’s recovery? Does the school offer a wilderness camp type of experience?
Here are some of the benefits all of us derive from interaction with nature:
People’s stress levels fell within minutes of contact with nature.
Hospital patients with views of nature needed fewer painkillers following operations.
Elderly people with easy access to nature are much happier with their quality of life.
Nature aids the part of the brain that controls irritability, helping to reduce violent behaviour.
Playing in a natural environment improved children’s concentration, self-discipline and their social and mental development, as well as reducing the symptoms of conditions like attention deficit disorder (ADHD).

Addicted to the Internet? You may have ADHD

Addicted to the Internet? You may have ADHD

A study performed at Kaohsiung Medical University in Taiwan set out to investigate the links between emotional conditions such as anxiety, depression and ADHD and Internet addiction. Two thousand fourteen students, 1204 male and 910 female, were assessed for all of the above factors using a self-report questionnaire.

The results showed that Internet addiction is associated with ADHD, depression, and hostility in males, while it is associated with ADHD and depression in females. Researchers noted that adolescent girls who had an Internet addiction didn’t display the hostility issues demonstrated by the adolescent boys. Social anxiety appeared to be a factor for both sexes.

Name that feeling: You'll feel better - Yahoo! News

Name that feeling: You'll feel better - Yahoo! News

CHICAGO (Reuters) - Putting feelings into words makes sadness and anger less intense, U.S. brain researchers said on Wednesday, in a finding that explains why talking to a therapist -- or even a sympathetic bartender -- often makes people feel better. ADVERTISEMENT



They said talking about negative feelings activates a part of the brain responsible for impulse control.

"This region of the brain seems to be involved in putting on the brakes," said University of California, Los Angeles researcher Matthew Lieberman, whose study appears in the journal Psychological Science.

He and colleagues scanned the brains of 30 people -- 18 women and 12 men between 18 and 36 -- who were shown pictures of faces expressing strong emotions.

They were asked to categorize the feelings in words like sad or angry, or to choose between two gender-specific names like "Sally or Harry" that matched the face.

What they found is that when people attached a word like angry to an angry-looking face, the response in the amygdala portion of the brain that handles fear, panic and other strong emotions decreased.

"This seems to dampen down the response in these basic emotional circuits in the brain -- in this case the amygdala," Lieberman said in a telephone interview.

What lights up instead is the right ventrolateral prefrontal cortex, part of the brain that controls impulses.

"This is the only region of the entire brain that is more active when you choose an emotion word for the picture than when you choose a name for the picture," he said.

He said the same region of the brain has been found in prior studies to play a role in motor control.

Researchers Light Up for Nicotine, the Wonder Drug

Researchers Light Up for Nicotine, the Wonder Drug

Smoking may be bad for you, but researchers and biotech companies are quietly developing pharmaceuticals that are decidedly good for brains, bowels, blood vessels and even immune systems -- and they're inspired by tobacco's deadly active ingredient: nicotine.

Nicotine acts on the acetylcholine receptors in the brain, stimulating and regulating the release of a slew of brain chemicals, including seratonin, dopamine and norepinephrine. Not surprisingly, the first scientific work that identified these chemicals and how they affect the body came out of nicotine research -- much of it performed by tobacco companies.

Now drugs derived from nicotine and the research on nicotine receptors are in clinical trials for everything from helping to heal wounds, to depression, schizophrenia, Alzheimer's, Tourette Syndrome, ADHD, anger management and anxiety.

"Nicotine is highly stigmatized -- and for good reason, because the delivery system is so deadly," says Don deBethizy, CEO of Targacept. "But the drug itself and the research generated by studying its effects on the brain both show great promise for helping us improve our physical and mental health."

DeBethizy worked for R.J. Reynolds Tobacco Company for 15 years -- he was one of the first to publicly declare that tobacco is addictive -- before he spun Targacept off as a separate company. RJR retains a 4 percent share of the Winston Salem biotech, which has one mission: to develop drugs that target the so-called "nicotinic receptors" in the human central-nervous system.

Nicotine performs that function to an unhealthy extreme. "Nicotine itself is hugely potent and not specific enough," says Linda Gretton, Targacept's director of communications. "But the research we have allows us to take the best therapeutic qualities of nicotine and develop treatments that target receptors."

Wednesday, June 20, 2007

A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence

A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence

A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence

M P Richards


Department of Archaeological Sciences, University of Bradford, Bradford, UK

Correspondence to: M P Richards, Department of Archaeological Sciences, University of Bradford, Bradford, West Yorkshire BD7 1DP, UK. E-mail: m.p.richards@bradford.ac.uk

Abstract


Knowledge of our ancestor's diets is becoming increasingly important in evolutionary medicine, as researchers have argued that we have evolved to specific type of 'Palaeolithic' diet, and many modern nutritional disorders relate to the mismatch between the diet to which we have evolved, and the relatively newer agricultural-based 'Neolithic' diets. However, what is the archaeological evidence for pre-agricultural diets and how have they changed over the four million years of hominid evolution? This paper briefly introduces the three lines of evidence we have for Palaeolithic and Neolithic diets; morphological changes, archaeological material evidence, and direct measurement of diet from bone chemistry. The morphological changes, increasing gracilization of the mandible and increasing brain size have been interpreted (based on analogies with living primates) as the move from plants to higher-quality, more digestible, animal meat, although this is debated. The archaeological evidence is especially weak, as many organic materials, especially plants, do not survive well, and are therefore invisible in the archaeological record. Artefacts, such as stone tools which are likely to be used for hunting and animal bones with evidence of human processing and butchering do indicate that hunting did occur at many times in the past, but it is impossible to judge the frequency. Direct evidence from bone chemistry, such as the measurement of the stable isotopes of carbon and nitrogen, do provide direct evidence of past diet, and limited studies on five Neanderthals from three sites, as well as a number of modern Palaeolithic and Mesolithic humans indicates the importance of animal protein in diets. There is a significant change in the archaeological record associated with the introduction of agriculture worldwide, and an associated general decline in health in some areas. However, there is an rapid increase in population associated with domestication of plants, so although in some regions individual health suffers after the Neolithic revolution, as a species humans have greatly expanded their population worldwide.

The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic

The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic

The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic

L Cordain1, S B Eaton2, J Brand Miller3, N Mann4 and K Hill5


1Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, USA

2Departments of Radiology and Anthropology, Emory University, Atlanta, Georgia, USA

3Human Nutrition Unit, Department of Biochemistry, University of Sydney, Sydney, New South Wales, Australia

4Department of Food Science, RMIT University, Melbourne, Victoria, Australia

5Department of Anthropology, University of New Mexico, Albuquerque, New Mexico, USA

Correspondence to: L Cordain, Department of Health and Exercise Science, Colorado State University, Fort Collins, CO. 80523, USA. E-mail: cordain@cahs.colostate.edu

Abstract


Objective: Field studies of twentieth century hunter-gathers (HG) showed them to be generally free of the signs and symptoms of cardiovascular disease (CVD). Consequently, the characterization of HG diets may have important implications in designing therapeutic diets that reduce the risk for CVD in Westernized societies. Based upon limited ethnographic data (n=58 HG societies) and a single quantitative dietary study, it has been commonly inferred that gathered plant foods provided the dominant energy source in HG diets.

Method and Results: In this review we have analyzed the 13 known quantitative dietary studies of HG and demonstrate that animal food actually provided the dominant (65%) energy source, while gathered plant foods comprised the remainder (35%). This data is consistent with a more recent, comprehensive review of the entire ethnographic data (n=229 HG societies) that showed the mean subsistence dependence upon gathered plant foods was 32%, whereas it was 68% for animal foods. Other evidence, including isotopic analyses of Paleolithic hominid collagen tissue, reductions in hominid gut size, low activity levels of certain enzymes, and optimal foraging data all point toward a long history of meat-based diets in our species. Because increasing meat consumption in Western diets is frequently associated with increased risk for CVD mortality, it is seemingly paradoxical that HG societies, who consume the majority of their energy from animal food, have been shown to be relatively free of the signs and symptoms of CVD.

Conclusion: The high reliance upon animal-based foods would not have necessarily elicited unfavorable blood lipid profiles because of the hypolipidemic effects of high dietary protein (19-35% energy) and the relatively low level of dietary carbohydrate (22-40% energy). Although fat intake (28-58% energy) would have been similar to or higher than that found in Western diets, it is likely that important qualitative differences in fat intake, including relatively high levels of MUFA and PUFA and a lower -6/-3 fatty acid ratio, would have served to inhibit the development of CVD. Other dietary characteristics including high intakes of antioxidants, fiber, vitamins and phytochemicals along with a low salt intake may have operated synergistically with lifestyle characteristics (more exercise, less stress and no smoking) to further deter the development of CVD.

European Journal of Clinical Nutrition (2002) 56, Suppl 1, S42-S52. DOI: 10.1038/sj/ejcn/1601353

Meat, cancer and dietary advice to the public

Meat, cancer and dietary advice to the public

Meat, cancer and dietary advice to the public

M Hill


Nutrition Research Centre, South Bank University London, UK

Correspondence to: M Hill, Nutrition Research Centre, South Bank University, 103 Borough Rd, London SEI OAA, UK.

Abstract


Background: It has been claimed for many decades that meat is a risk factor for colorectal cancer, and that it has no compensating benefits in terms of cancer risk. The evidence for this has been critically reassessed.

Methods: The epidemiological evidence, particularly that produced in recent years, has been re-examined to determine whether it is sufficiently consistent to warrant giving firm advice to the general public.

Results: Far from being supportive, the epidemiological data does not justify this claim. A large mass of evidence is presented from case-control studies and prospective studies, in which the data from Europe are not consistent with those from the United States. This is because of the different contexts (in terms of meal composition) within which meat is consumed in different countries. In fact the epidemiological data are much more consistent with there being a protective role for fruit, vegetables and whole grain cereals and no role for meat in colorectal cancer, and a protective role in gastric cancer.

Conclusions: Meat is a good source of protein, readily available iron, calcium, magnesium, selenium, zinc and a range of B vitamins. Since the evidence for any role in colon carcinogenesis is so weak, and since such a high proportion of women of child-bearing age are iron deficient, the consumption of meat, as part of a balanced and varied diet, should be actively encouraged.

European Journal of Clinical Nutrition (2002) 56, Suppl 1, S36-S41. DOI: 10.1038/sj/ejcn/1601352

I have the hla-dbq1*0301 and 0602 genes, one of which predisposes to gastric cancer. Magnesium and zinc deficencies are asssociated with ADD