The Hungry Brain and Energy Density

Part 1 Part 2

One way our ancestor Hominids used to provide their ever hungry and growing brain with calorie-dense and nutrient-dense foods was to become more carnivorous. It worked, but the scientists were bothered with the question: could there be an alternative way?

Harvard University researchers suggested that cooking could play as important a role. It probably happened almost 2 millions years ago. Cooking plant foods made them softer and their "bioavailability" increased. This allowed for saving the cranial space for bigger brains rather that for huge teeth needed before to tear apart raw meets.

Higher energy density made possible energy-costlier activities like hunting. The matter is, the growing areal of grassland caused increase in numbers and diversity of grazing animals. There are signs of this exact behavior in the form of gazelle bones and butcher tools at the hominid campsites of that time.

Researchers consider these signs an important evidence of hominid diet changes toward greater stability and diversity. So they ate better and their brains grew bigger -- creating a positive synergistic feedback in human evolution.

All these facts are seen by scientists as reasons of spreading the Homo erectus from Africa to Georgia (Black Sea,) China, and Indonesia (Java) while Homo habillus and Australopithecus remained in the areas of Chad, Ethiopia, Kenya, Tanzania, and in South Africa. Further inventions such as farming with plant quality improving as well as animal domestication and breading continued the line of improving the quality and stability of human diet.

Where does it leave us now? Yes, human race survived, multiplied, and spread all over the world. However, the energy dynamics established for the species in need of significant energy expenditures remains though this same species (at least the developed part of it) don't need that much energy any longer. Now, we face the dilemma: we can get all nutrients that our big brains need only coupled with too many calories for our dramatically changed life style.

Most fats seem to be protective against Alzheimer disease

In 1989-99, an association was found, between dietary fat composition and cognitive performance in later adult years: the higher intake of monounsaturated and polyunsaturated fats and the lower intake of saturated fat -- the higher cognitive performance. Another, epidemiologic study conducted in 1997 suggested that high intake of total fat, saturated fat, and dietary cholesterol may increase the risk of dementia.

However, researchers at St Luke's Medical Center, Chicago, Ill found increased risk of Alzheimer's disease among people with high intakes of saturated and trans-unsaturated fats and decreased risk with high intakes of polyunsaturated and monounsaturated fats. Consumption of vegetable fat and a high ratio of polyunsaturated to saturated fats were also protective, whereas total fat, animal fat, and dietary cholesterol had no association with Alzheimer disease.

Sources

Brain Res. 1989;505:302-305

Behav Neurosci. 1996;110:451-459

Behav Brain Res. 1999;101:153-161

Am J Epidemiol. 1997;145:33-41.

Arch Neurol. 2003;60:194-200

Why is fat so tasty?

Most animals, including humans, prefer high-fat food to low-fat food. Fatty foods are very palatable though the fatty acids, which make these foods fatty, are tasteless. On the other hand, sweet, sour, salty, or bitter foods are recognized by the corresponding receptors of the taste buds. The receptors then send information to the brain areas responsible for positive or negative sensations called hedonic or aversive. But how the tasteless fatty acids manage to make fatty foods so tasty?

Recently, it was suggested that long-chain fatty acids attaching to their specific transporter in the tongue. These long-chain fatty acids are recognized on the tongue, and then neuropeptides and neurotransmitters such as the famous "reward chemical" beta-endorphin is released in the brain.

Source: J Nutr Sci Vitaminol (Tokyo). 2007 Feb;53(1):1-4.

The ketogenic diet in a pill: "as elusive as ever"

Jong M. Rho and Raman Sankar. Barrow. The ketogenic diet in a pill: Is this possible? Epilepsia Volume 49 Issue s8, Pages 127 - 133 2008

Over the past decade, much progress has been made in
understanding the mechanisms of ketogenic diet (KD) action. From the
complex systemic and metabolic changes induced by the KD have emerged
innovative hypotheses attempting to link biochemical adaptations to its
clinical effects. Despite such developments, the fundamental question
of how the KD works remains as elusive as ever. At present, it is
unclear which of the many potential mechanisms proposed thus far are
directly relevant to the clinical effects of the KD. It is unlikely
that these numerous hypotheses can be unified into a single mechanism
(or a final common pathway). Nevertheless, it may be instructive to
consider each of these putative mechanisms in turn and ask the
following question: if the mechanism or target in question is a
critical determinant of the anticonvulsant efficacy of the KD, then
would a similar intervention known to be based on that mechanism yield
a comparable effect? Perhaps answering this question for each
mechanistic speculation might help substantiate (or invalidate) that
particular hypothesis. Can the KD be packaged into a pill? At present,
the answer is likely “no.” We have yet to discover a “magic bullet”
that completely mirrors the anticonvulsant (and potential
neuroprotective) effects of the KD. However, without a clearer
understanding of the mechanistic elements comprising the complex
metabolic puzzle posed by the KD, we would be left only with empiric
observations, and to wonder curiously how a high-fat diet can exert
such profound clinical effects.

Neurological Institute and St. Joseph’s Hospital and
Medical Center, Phoenix, Arizona, U.S.A. ; and David Geffen School of
Medicine and Mattel Children’s Hospital UCLA, University of California
Los Angeles, California, U.S.A.

Epilepsy Drugs May Treat Alzheimer's

(WebMD) A group of drugs used to treat epilepsy may also treat Alzheimer's and Parkinson's disease.

New research shows treatment with T-type calcium channel blockers, used to treat epilepsy, protected nerve cells from the brains of mice that can be damaged by neurodegenerative disorders such as Alzheimer's and Parkinson's disease.

Researchers say there aren't any effective medications that protect brain cells from age-related damage and degeneration. If these findings hold up under further study in humans, they could lead to a new class of more effective treatments for age-related neurological diseases.

Calcium-signaling pathways play an important role in the survival of nerve cells (neurons) in the brain. As people age, this process can become disrupted and can lead to cognitive and functional decline.

Researchers say that opens up the possibility of using chemicals like calcium channel blockers that are involved in the calcium-signaling process to protect the nerve cells from death.

The study, published in Molecular Neurodegeneration, looked at the effects of treatment with calcium channel blockers on the brain cells of mice.

Researchers found neurons showed an increase in viability after treatment with the calcium channel blockers over both the long term and short term.

"Our data provides implications for the use of this family of anti-epileptic drugs in developing new treatments for neuronal injury, and for the need of further studies of the use of such drugs in age-related neurodegenerative disorders," says researcher Jianxin Bao, PhD, of Washington University in St. Louis, in a news release.