Archive for July, 2016

HCG Rapid Weight Loss Diet FAQ

Friday, July 29th, 2016

HCG Diet Frequently Asked Questions (FAQ)

HCG is a hormone that is naturally produced in the body. HCG diet drops are a relatively new product based on the classic diet protocol developed by Dr. Simeons in the 1950s. The HCG diet protocol has been used by thousands, perhaps hundreds of thousands of people, to effectively tell the body to use stored fat as energy and help individuals lose weight.

Many people who hear of HCG diet drops and the HCG diet for the first time have questions. Following are some of the most common questions we hear.

Is HCG safe?

HCG diet drops are completely safe to take. HCG is a hormone naturally produced in women during pregnancy. Many pregnant women experience incredibly high surges of HCG with no adverse effects. Some HCG dieting products contain small amounts of HCG, with a correspondingly small risk of side effects. Other HCG dieting products do not contain any HCG, but are specially designed to mimic the HCG hormone, resulting in shedding of excess weight with no side effects from the HCG product itself.

Will HCG make men feminized?

HCG is a hormone produce by women during pregnancy. It’s also used as a medication to promote fertility in women. A less well known use of HCG is to promote sexual development in boys with underdeveloped gonads. But regardless of HCG’s uses, the amount of HCG that is used for weight loss is too small to have such effects anyway. Men will not become feminized by using HCG for weight loss.

Who can use the HCG diet?

Almost all individuals, male, female, old and young are able to use the HCG diet, with some exceptions. People who should not use the HCG diet include: those with a BMI less than 20, pregnant or nursing women, children under the age of 18, and anyone with serious health problems (for example, heart disease, cancer, kidney disease, liver problems, or type one diabetes). You should always check with a naturopath at New Leaf before starting any diet or exercise program.

Can I just get on a low calorie diet without HCG?

On the HCG diet, you will be eating just 450-500 calories a day while taking HCG diet drops. HCG diet drops are intended to decrease hunger and prevent common symptoms of very low calorie diets, all while recalibrating your hypothalamus and your metabolism. You can eat just 500 calories a day without taking HCG diet drops, but you will simply be starving yourself—it’s miserable. If you go on a diet that has you eating more calories, you most likely will not lose as much weight. For best results, HCG and the 500 calorie diet are both required.

What about hunger on the 500-calorie diet?

Many experience no hunger at all on the HCG diet. Hunger can occur in the first week or two of the HCG diet; however, after about the second week, even very small portions will likely start to make you feel full. This is due to the huge amounts of calories your body is getting from its stored fat reserves. Hunger during the first week can often be eliminated by following the two initial loading days properly. Occasional hunger during the rest of the diet can occur, but there are strategies to deal with it effectively.

Why is there so much controversy over the HCG diet?

There are a few reasons for controversy. First, HCG has never been approved for weight loss. However, Dr. Simeons’ diet has many thousands of success stories, leading doctors prescribe it to their patients off-label and encouraging dieters to seek out alternative products like homeopathic HCG. The bottom line is that the diet really works for many people.

Secondly, the fact that the HCG diet is a very low calorie diet causes some heartburn among conservative nutritionists and doctors. But the truth is that very low calorie diets that provide high-quality protein and proper nutrition (like the HCG diet) have been shown to be perfectly safe for healthy individuals. The best HCG suppliers will provide multivitamin supplements along with the diet, as well as higher-calorie plans for those who need or desire them.

Finally, many individuals have known of weight loss scams and are skeptical of anything that might just be a fad. But fad or not, you can’t argue with results. As with most things in life, there is no one size fits all diet. HCG works for a lot of people. Maybe it will work for you, too.

HCG Diet and Exercise: recommendations and guidelines

Friday, July 29th, 2016

HCG Diet and Exercise: Guidelines, Warnings and Recommendations

Weight gain during HCG is frustrating – this is why we recommend VLA BioImpedance Screenings every week or two so that you KNOW what is going on in your body….  This article explains WHY we can have a temporary weight gain with exercise.  Knowledge is power.  Know what is going on in your body – and then the motivation will continue!

As with most things, there are multiple views on whether exercise should be incorporated as part of the HCG diet. Even among those who do recommend exercise, there is no consensus on the intensity, duration, frequency, and types of exercise that should be included.

On the HCG diet it is completely possible to lose a significant amount of weight with very little exercise, or even without exercising at all. In fact, some clinics and practitioners recommend absolutely no exercise. For many dieters, especially those who detest physical activity, this is one of their favorite features of the HCG diet. Many dieters have been told that told repeatedly that their weight problems are mostly caused by laziness or lack of exercise. It can certainly feel relieving to be “allowed” or advised to avoid exercise.

The extra fat deposits you are trying to rid yourself of through the HCG diet are great deposits of energy. While on the HCG diet, your body will be breaking down these deposits. The presence of HCG allows this breakdown to occur more easily. Vigorous exercise demands quickly available energy. Even though your body will have a lot of potential energy from fat deposits more readily available, the energy from it cannot be metabolized quickly enough to supply heavily utilized muscles.

Most HCG dieters will track their weight closely. Weighing in daily, or sometimes multiple times per day. Increases in weight during phase 2 of the HCG diet can be alarming. How can you gain weight when only consuming 500 calories in a day?! The breakdown of muscles that occurs from intense workouts can and usually will cause inflammation in the affected muscles. Your body will absorb additional water to aid in the repair of these muscles and this extra water can easily show up in increased weight from one day to the next. The weight will almost always level out over time, but the psychological effect of the temporary weight increase can be difficult for dieters.

Dr. Simeons recommended only light exercise such as walking and light biking. This exercise should only be done at low intensity and for fairly short periods of time. He noted the weight gain caused by vigorous exercise in this way:

“…the weight can temporarily increase — paradoxical though this may sound — after an exceptional physical exertion of long duration leading to a feeling of exhaustion. A game of tennis, a vigorous swim, a run, a ride on horseback or a round of golf do not have this effect; but a long trek, a day of skiing, rowing or cycling or dancing into the small hours usually result in a gain of weight on the following day, unless the patient is in perfect training. In patients coming from abroad, where they always use their cars, we often see this effect after a strenuous day of shopping on foot, sightseeing and visits to galleries and museums. Though the extra muscular effort involved does consume some additional calories, this appears to be offset by the retention of water which the tired circulation cannot at once eliminate.”

Dr. Simeons also noted that patients who insisted on exercising vigorously while on the program often overate because of exercise-induced hunger, stalling weight loss or even leading to weight gain. Many practitioners and dieters take this statement to mean that all exercise is forbidden during phase 2.

Exercise is not forbidden but must be undertaken with great care during the strict diet (Core Phase or Phase 2). Deliberate workouts during the HCG diet should be tailored to each individual’s capabilities. Each person will have a different level of fitness, different strengths, different preferences, and different abilities.

A dieter with a body that is already accustomed to intense exercise will be able to handle exercise much more easily than one who is very out of shape. A fit body will not sustain as much intramuscular damage and its associated inflammatory effects from exercise that a non-fit body would.

In general it is good to take a very cautious approach to exercise while on the HCG diet. You will be taking in very little food, very little fuel for your body to use to power your muscles during exercise. Fat will be released and metabolized for energy, but carbohydrates are a much more easily and quickly metabolized fuel. They are the body’s main source of energy especially during very intense and very long duration exercise. Without them, exhaustion and fatigue occur much more quickly, often along with dizziness and shortness of breath. Another side effect of lack of carbohydrates during vigorous exercise is an extremely strong feeling of hunger, usually with cravings for carbohydrate-laden foods. All of this can work together synergistically against the dieter. An exhausted, light-headed person has a much harder time resisting the body’s increased demands for carbohydrate rich foods!

If you are used to intense exercise already, you can try to continue with what your are doing, but most likely you will lack the necessary energy and/or will not recover as quickly as usual while you are on phase 2 of the HCG diet. If you are not used to intense exercise, do not attempt it during the HCG diet!

If you are used to light or moderate exercise, you may continue as before, possibly shortening the duration or intensity of your workouts as necessary. As with intense exercisers, watch for overtraining and energy levels. Dial down your training if you see any signs of it.

If you are not used to exercise, now is probably not the best time to start.

Some Sample Exercises During Phase 2

Low Intensity (OK for everyone, but always monitor for signs of overtraining)

  • Walking
  • Bicycling
  • Yoga
  • Gentle swimming
  • Lawn mowing

    Medium Intensity (Only for those already accustomed to medium intensity workouts monitor for overtraining)

  • Jogging
  • Snow shoveling
  • Lap swimming
  • Moving furniture

    High intensity (Not Generally Recommended for Phase 2 of HCG Diet)

  • Heavy weight training
  • Running
  • Crossfit
  • Triathlons
  • Sprinting

WINTER: Colds, flu, coughs and sniffles! There’s help at New Leaf 3348 6098

Tuesday, July 26th, 2016

Focus On: Issue 3 2016

Winter is typically the season of colds, flu, coughs and sniffles, but it doesn’t have to be. In this article, we shall discuss how to avoid and ameliorate the acute respiratory infections characteristic of this time of year.

Build Your Defences

If there is such a thing as an “immunity nutrient”, then it has to be zinc. Zinc levels are tightly regulated and when this mechanism is disturbed, zinc availability is reduced, leading to immune impairment.4 Zinc deficiency affects the survival, proliferation and maturation of all cells involved in both innate and adaptive immunity (monocytes, neutrophils, natural killer-, T-, and B-cells).T cell functions, and the balance between the different T helper cell subsets, are particularly susceptible to changes in zinc status. Even slight deficiency causes polarization of immunity to pro-atopic Th2 dominance, with loss of antiviral defence.6 Zinc with Vitamin C Powder provides therapeutic levels of zinc with additional nutrients such as vitamin C and betacarotene, for the ultimate nutritional combination for prophylactic and acute immune support.

Feverish Counterattack

Fever is the first part of the body’s counterattack. As soon as an infection is detected, cytokines are generated which trigger the liver to commence the acute phase response (APR), part of which involves the production of acute phase proteins (APPs) that prepare the body for defence. Although nonspecific, the APR is central to the innate immune response, helping to prevent infection, clear potential pathogens, initiate inflammatory processes, and contribute to resolution and the healing process.

One of the defences activated by the APR is the generation of heat to raise body temperature, i.e., fever. The increased body temperature impairs invader metabolism, such as viral replication, and up-regulates host metabolism.7

Blocking fever and the APR with non-steroidal anti-inflammatory drugs (NSAIDs) interferes with antigen processing and may impair development of full immunity to that invader.8 You can, however, encourage the body to process the invader quicker. Herbs that do this are called febrifuges or antipyretics, and one of the most useful is elder (Sambucus nigra). The ability to resolve fever suggests a capacity to resolve the cause of the fever, i.e., the viral invader itself; and indeed, elderberry has been found to be potently antiviral.9

From a traditional Chinese medicine (TCM) point of view, bitters such as Andrographis paniculata and Picrorrhiza kurroa, as featured in NK Cell Regulation, are ‘cooling’, and in fact they have been shown to be antioxidant and anti-inflammatory, and have been traditionally used to reduce fevers.10, 11, 12 These herbs are intensely bitter and are commonly used for liver and digestive complaints, but are also very effective for virally-driven upper respiratory tract infections (URTIs). 13, 14 There may be a connection here, in that the liver is the organ that orchestrates the APR. Elder, andrographis, picrorrhiza and zinc may all be found in NK Cell Regulation to enhance patients’ immunity and reduce the severity and duration of upper respiratory infections.

Regain Your Strength

The APR and associated immune mechanisms use a lot of energy – with the white blood cells busily patrolling, each requiring the energy to do so. Research has shown co-enzyme Q10 may potentially be useful in fuelling immune responses. 15

Further bolstering of the immune system may be garnered from the use of Cordyceps, Coriolus and Reishi for Immune Stimulation, which features oriental medicinal mushrooms such as Cordyceps sinensis, used in TCM for strengthening the immune system and to manage respiratory disorders. Ganoderma lucidum (reishi) has been used to enhance immune activity in people who suffer from frequent or chronic infections. 16 Lentinula edodes (shiitake) can boost resistance and protection against respiratory viral infections such as influenza, probably via induction of interferon. 17

Don’t let your patients succumb to the misery of coughs and colds this winter. Following the simple steps detailed here will support your patients’ immune defences against infection, promote their immune response, and rebuild their immunity after infection. Bring on the winds of winter – we’re ready for them!

LEAP: The Learning Enhancement Acupressure Program – by Dr Charles T. Krebs

Tuesday, July 26th, 2016

We’ve been doing kinesiology at New Leaf Natural Therapies for 20 years.  LEAP is an integrative approach to supporting better brain function – for moods, stress, survival patterns, learning problems, damaging behaviours, anxiety, suicidal thoughts…

LEAP®: The Learning Enhancement Acupressure Program: Correcting

Learning and Memory Problems with Acupressure and Kinesiology.

By Dr. Charles T. Krebs

ABSTRACT:

The Learning Enhancement Acupressure Program, or LEAP®, has been developed since 1985 inconjunction with clinical psychologists, speech pathologists, neurologists and other health professionals, as a very effective program for the correction of most learning difficulties. LEAP® is based on a new model of learning integrating recent concepts in neurophysiology of the brain and uses highly specific acupressure formatting to address stress within specific brain structures. The application of specific non-invasive acupressure and other energetic techniques can then resolve these stresses resulting in a return to normal function.

In the LEAP® model of learning Gestalt and Logic functions are not simply localised in the right or left cerebral hemisphere as in the popular Right Brain/Left Brain model of learning. But rather, each type of conscious brain function or process appears to have a cerebral “lead” function that is either predominantly Gestalt (Visuo-spatial, Global) or Logic (Linear, Sequential) in nature. These cortical “lead” functions provide a “point of entry” into a widely distributed system comprising many subconscious cortical sub-modules in both hemispheres and many subconscious subcortical modules throughout the limbic system and brainstem.

While the Gestalt and Logic “lead” functions are conscious, these functions are dependent upon many levels of subconscious sensory processing at many levels within the nervous system. While this processing through multiplexing and parallel processing at many different levels is highly efficient, it means that brain processing is “time bound”. Since many components of any mental function are performed in many different parts of the brain, and often at different speeds, coherent output in the form of “thinking” requires integration and synchronisation of all of these separate processes.

Loss of integrated brain function, termed loss of Brain Integration in LEAP®, thus results in the loss of a specific mental capacity, the ability to perform a specific type of mental task. When these specific mental capacities are required for academic performance, their loss can result in Specifi Learning Disabilities.

Specific Learning Disabilities (SLDs) arise in this model by either lack of access to specific subconscious processing modules, either cortical or subcortical, or the de-synchronisation of neural flows in the integrative pathways linking processing modules. Thus to resolve SLDs, you need only “open up” access to the “blocked” processing modules or re-synchronise the timing of information flow between them to re-instate integrated brain function.

The LEAP® program provides an integrated acupressure protocol using direct muscle biofeedback (kinesiology) as a tool to identify “stress” within specific brain nuclei and areas that have “blocked” integrated function. The application of the LEAP® acupressure protocol using acupressure and other energetic based techniques to re-synchronise brain function resolves learning and memory problems in a high percent of cases.

HISTORY OF SPECIFIC LEARNING DIFFICULTIES.

Difficulties with learning academic tasks such as reading, spelling and mathematics have been recognised for over a century, with Kussmaul in 1877 ascribed as the first person to specifically describe an inability to read, that persisted in the presence of intact sight and speech, as word blindness.1 The word dyslexia was coined by Berlin in 1887.2 Within a decade a Glasgow eye surgeon James Hinschelwood (1895) and a Seaford General Practitioner Pringle Morgan (1896) observed students who were incapable of learning to read and hypothesised that this was based on a failure of development of the relevant brain areas which were believed to be absent or abnormal.

This model was based on the assumption that developmental dyslexia (congenital dyslexia) was similar in form to acquired dyslexia, which is dyslexia due to brain damage after a person has already learned to read. Deficits in other types of learning, such as mathematics, would also result from some other underlying brain damage or abnormality.3

Work in the early part of the twentieth century, particularly by Samuel T. Orton in the 1920s and 1930s suggested that learning difficulties such as dyslexia were not based on anatomical absence or abnormality, but rather it was delay in the development of various areas that caused these dysfunctions. This belief was largely ignored until the 1960s when it was revived by a growing interest in neuropsychology. However, more recent developments in neuropsychology and neurophysiology support the hypothesis that dysfunctions within the brain, both anatomical and developmental, may be causal in many learning problems.4

It was not until 1963, in an address given by Samuel Kirk, who argued for better descriptions of children’s school problems that the term “learning disabilities” originated. Since that time there’s been a proliferation of labels that attempt to dissociate the learning disabled from the retarded and brain damaged.

Definitions

In the context of this synopsis, Specific Learning Disorders or Disabilities (SLDs) relates to problems with physical co-ordination and acquiring the academic skills of reading, writing, spelling and mathematics including both Dyslexia and Attention Deficit Disorder (ADD) with or without hyperactivity. ADD with hyperactivity is now commonly called Attention Deficit Hyperactivity Disorder (ADHD) or hyperkinetic disorder in Europe. Historically, Dyslexia has been widely defined in terms of deficits in the areas of reading, spelling and language. However, more recent conceptualisations have included a definition that also encompasses a wide range of problems, including clumsiness and difficulty with rote learning.5 Fawcett and Nicolson have also challenged the prevailing hypothesis that Dyslexia is merely a language based problem, suggesting that it might be a more generalised deficit in the acquisition of skills.6

The term Dyslexia is not defined in the DSM IV (1994) although it is still commonly used in literature discussing various learning difficulties. The term Learning Disorders (DSM IV) currently encompasses various types of learning difficulties including dyslexia and Attention Deficit Disorder (ADD). Learning Disorders are defined in the DSM IV as being essentially a persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than is typically observed in individuals at a comparable level of development. The performance of these individuals on standardised tests for reading, mathematics, or written expression is substantially below, more than 2 standard deviations (SDs), same age peers even though their IQ scores are average or above average.7

Incidence

Frequently, children diagnosed as learning disabled are also inattentive and deficient in linguistic skills, most often in reading.8 Rutter and Yule examined a large population of children from a number of different studies and found 3.5% of Isle of Wight 10-year-olds, 4.5% of 14-year-olds and over 6% of London 10-year-olds showed reading difficulties.9 Gaddes looked at the proportion of children with learning disorders in various studies in both North America and Europe and found that the need for special training for learning disorders ranged between 10-15% of the school age population.10 However, estimates of the prevalence of learning disorders for broad age ranges is problematic because a learning disability is an emergent problem that is often not evident until later years in schooling. Using the criteria of defining learning disorders as being two years behind on standardised tests, less than 1% of 6-year-olds are disabled, 2% of 7-year-olds and so on until at age 19, 25% would be classified as learning disabled. So these children fall progressively behind as they mature and the complexity of work increases.11 In an address given by the Australian Federal Schools Minister, Dr David Kemp, in October 1996, Kemp stated that a study of 28,000 students in four surveys in Australia found 30% of year 9 students lacked basic literacy skills. This high incidence of learning disorders in school children indicates a need for effective treatment. Studies in other countries, both English, French and German support these figures, so specific learning difficulties, which cover all types of learning disabilities from dyslexia, reading problems, ADD to ADHD, probably represent greater than 15% of school-aged children, and may be as high as one third of all school-aged children.

Causes

Currently hypotheses concerning learning disorders suggest that they are primarily the result of one or more of five major factors;

1) structural damage,
2) brain dysfunction,
3) abnormal cerebral lateralisation,
4) maturational lag and
5) environment deprivation.

While none of these theories is unequivocally supported by current data, all of these factors may contribute in varying degrees to learning disabilities.12

Brain damage and overt brain dysfunction would appear to account for a relatively small percentage of children with learning disorders. The great majority of other children with learning disorders do not typically show many of the neurological symptoms associated with brain damage in adults. For instance, EEG and CT studies have not shown structural damage and abnormal EEGs correlated with known brain damage are not consistently observed in children with learning disorders.13 Rather than direct brain damage, there is evidence that abnormal physiological or biochemical processes may be responsible for malfunction in some part of the cerebral cortex.

Electrophysiological recording studies have associated specific high frequency EEG and AEP (averaged evoked potentials) abnormalities with various types of learning disorders.14 Recent studies with SSVEP (Steady state visual evoked potential) have shown that children diagnosed with Attention Deficit Disorder demonstrate similar abnormal SSVEP patterns when compared to normal subjects while performing the same cognitive task.15 The brain dysfunction hypothesis suggests that the dysfunction may be a consequence of defective arousal mechanisms resulting in some form of inadequate cerebral activation.16

This is supported by studies of children with learning disorders that show they have difficulty on continuous performance tests requiring attention and low distractibility; had slower reaction times to stimuli, and increased errors due to impulsivity on tests of visual searching.17 Douglas proposed that the deficits on these tasks resulted from inadequate cerebral activation. Learning disorders of some types at least, do improve with drugs like amphetamines that cause cerebral activation via increasing subcortical arousal. In fact this is the basis of treating hyperactive children with Ritalin.18

An alternative model of learning disorders is based on recent neurophysiological findings that suggest it is the timing and synchronisation of neural activity in separate brain areas that creates high order cognitive functions. Any loss or malfunction of the timing mechanism may cause disintegration of neural activity and hence dysfunction in cognitive tasks.19 Clearly, brain dysfunction due to inadequate cerebral activation may indeed lead to disruption of the timing and synchronisation of neural flows, and thus these two hypotheses may just be different aspects of the same process.

This model supports the approach in the Learning Enhancement Advanced Program (LEAP®) that Dr. Krebs developed in the late 1980s early 1990s.20 In the LEAP® Model, Specific Learning Disorders are based on the disruption or loss of timing and synchronisation between the neural activity in the diverse brain regions, both cortical and subcortical, that must be synchronised in order for successful integration to produce normal cognitive activity. Learning disorders would arise in this model from a lack of integration of functions that occur simultaneously in separate brain regions.

If the brain does integrate separate processes into meaningful combinations we call ‘thought’ or cognitive ability, then the main risk is mis-timing or loss of synchronisation between these processes. To quote Damasio “any malfunction of the timing mechanism would be likely to create spurious integration or disintegration”.21 For synchronous firing of neurons in many separate brain areas to create cognitive functions would require maintenance of focused activity at these different sites long enough for meaningful integration of disparate information and decisions to be made.

THE LEAP® MODEL OF LEARNING:

From a review of the major brain structures and the workings of learning and memory in the neurological literature, it is clear that both memory and learning do not involve a single, global hierarchical system in the brain. But rather, learning involves interplay between many inter-linked sub-systems or modules.22 Also, the timing and synchronisation of information flow between these sub-systems and modules appears to be critical to the success of learning and coherent cognitive function.

However, the sub-systems or modules underlying both learning and memory are both conscious and subconscious with most of the early leveling processing being totally subconscious, and only the highest levels of neural processing reaching consciousness. Yet, it is indeed these conscious modules that initiate and direct the processing to be done by the subconscious modules, as both learning and memory require “conscious” effort to occur. This means that the memory and learning processes can be disrupted at both the conscious and subconscious levels, depending upon which neural substrates or integrative pathways are disrupted.

Sensory processing of all types is initially a relatively linear chain of neural impulses originating from a generator potential of the sensory receptor, and following a chain of neurons into the Central Nervous System (CNS) and brain. However, this initially linear stream of nerve impulses, the data of the CNS, rapidly becomes divergent and multiplexed at higher levels of cortical processing.

Conscious perception only arises at the highest levels of these multiplexed data flows as they are reintegrated back into unified conscious perception by the cortical columns directing all conscious brain activity. Thinking and other cognitive abilities rely upon all of the proceeding levels of subconscious sensory processing, which are predominately bilateral initially, but which become progressively asymmetrical and lateralised with increasing levels of conscious awareness. Sensory information is processed initially as neural flows of increasing complexity that generate preverbal images and symbols, but becomes increasingly defined by language in higher level cognitive processes. And language by its very nature is based upon abstract representations of external reality (called words), that follow linear rules (grammar), and word order linked to meaning (syntax). Hence it is predominately sequential and linear in form, which permits analytical evaluation of the thoughts generated following rational rules of Logic. From the perspective of Logic, the world is interpreted as parts that can be constructed into a whole via deductive reasoning.

Sensory and other mental data not suitable for language-based rational processing is processed via visuo-spatial image and symbols that permit global, holistic comprehension of the whole and is inherently non-rational.23 This global, simultaneous, non-rational visuo-spatial processing has been termed Gestalt (German for pattern or form), with the meaning of the whole extracted via inductive reasoning. From the Gestalt perspective, the world is seen as a “whole” with intuitive understanding of the properties of the whole. There is no rational analysis of “Why?”, it just “Is”.

In the LEAP® Model of Learning, it is recognized that most of the lower level linear sensory processing occurs below conscious perception, that is either subcortical, being processed in the brainstem or other brain nuclei like the hypothalamus, thalamus, basal ganglia, etc., or is palaeocortical and limbic. Even the basal levels of cortical processing are largely bilateral and subconscious, and thus occur outside of conscious perception. All higher level cortical processing, which may become conscious, is thus reliant upon maintenance of integrated function and neural flows at these subconscious levels.

However, the more overtly cognitive components of learning rapidly become lateralised with processing dominated by activation of cortical columns, the functional units of the neocortex, in one hemisphere of the brain or the other. In right-handed people, Logic processing typically activates cortical columns in the left hemisphere, that then process the data in a linear analytical way, while activation of cortical columns in the right hemisphere process data in a Gestalt, visuo-spatial way.

Thus, at the highest levels of conscious neural processing underlying cognition and thought, whether that “thought” be verbally based language of Logic, or global intuitively based “knowing” of Gestalt, the neural processing is highly lateralised and is predominately processed in the right or left hemisphere.

The neural substrates for all “conscious” functions therefore are cortical columns of the neocortex (Fig. 1). Conscious activation of a cortical column acts to initiate a cascade of neural flows that rapidly spread to other cortical areas both conscious and subconscious in both hemispheres, and also into many subcortical structures as well. These consciously activated cortical columns initiate either Gestalt or Logic functions depending in which hemisphere they are located.

In LEAP® we term cortical columns activating Logic functions, Logic “lead” functions, and those activating Gestalt functions, Gestalt “lead” functions. These “lead” functions provide points of entry into an inter-linked set of cortical and subcortical modules that then perform our mental functions.

Figure 1. Cortical Columns. Vertical slabs of cortex consisting of all six distinct cell layers, called cortical columns, are the functional units of the cerebral cortex. Some of the cells like the large pyramidal cells have dendrites that extend through almost all layers and axons that exit the gray matter to become part of the white matter tracts carrying information to other parts of the brain and body. There are also innumerable interneurons connecting the cells within each cell layer and between the layers.

Indeed, it was a misunderstanding about the nature of these “lead” functions from which the popular “Right Brain – Left Brain” model of learning and brain function arose. Because damage to specific cortical columns caused loss of specific conscious functions, e.g. the ability to form an image, or figure out certain types of problems or solve certain types of puzzles, it was assumed that the damaged area actually did that specific function. In reality, all that cortical column did was provide a point of entry into these inter-linked sets of cortical and subcortical modules that actually performed the function lost because of the damage to the cortical “lead” function.

An analogy would be damage to the “K” key on your keyboard. Your consciousness is still intact and able to initiate “K” questions, and your computer system is still able to process and answer “K” questions, but the interface to initiate “K” processing in the computer has been damaged. Like wise, if a Gestalt “lead” function is damaged, the process initiated by this “lead” function no longer activates the inter-linked cortical and subcortical functions that are required for this process to occur. Thus, while damage to the area initiating a function, “blocks” the rest of the processing needed to perform the function, the area initiating function never actually ever “did” the function in the first place. To continue this analogy, in most cases it is not overt “damage” to the cortical “lead” function or subcortical brain areas that prevents effective thinking, but rather “blocked” access to these brain areas due to some stressor that is the problem. Thus, much in the same way a “sticky” key blocks fluent typing, “blocked access” to specific brain areas blocks effective thinking and problem-solving.

Synopsis of the LEAP® Model of Learning:

In summary, the LEAP® Model of Learning is based on the following suppositions about the nature and location of neural processing underlying learning and memory:

Sensory processing initiated by sensory receptors generates initially linear neural flows that rapidly diverge at each successive processing centre (spinal and cranial nerve ganglia, brainstem nuclei, subcortical nuclei, limbic cortices, and finally neocortical columns) into a number of different complex data streams. All processing below the neocortex is subconscious.

Each processing centre, at each successive level within the spinal cord, brainstem, diencephalon, basal forebrain and cortex elaborates the sensory data, defining some aspect more than another, or adds additional types of information needed to define the sensory data further at the next level of processing. All processing below the neocortex is subconscious.

At the higher cortical levels, input from many lower levels both cortical and subcortical is integrated to form a conscious perception of the initial sensory experience.

These higher cortical levels not only integrate processing of the “raw” sensory data, but also include integration of input from memory areas about past experiences with similar sensory stimuli.

At the highest cortical levels the conscious perceptions formed at lower cortical levels are further processed asymmetrically in either Gestalt or Logic cortical columns, and hence perceived as a visuos-patial pattern or a Gestalt, or abstractly as a verbal word based language or an abstract symbol based mathematical language.

The very highest levels of conscious processing that underlie our thinking about conscious perceptions, while dependent upon input from all areas of the brain, are generally frontal lobe and particularly involve working memory areas in the Dorsolateral Frontal Cortex.

A whole set of basal brainstem mechanisms maintain the organism in a state of homeostasis, such that higher level conscious sensory processing can proceed effectively:

These include the Reticular Activating System, the Periventricular Survival System, the Vestibular System and the Sensory-Motor System. Imbalances within or between these systems may disrupt on-going sensory processing and integration at this and higher levels. Processing at this level is totally subconscious.

The initial “raw” data stream is “sampled” by the Amygdala and other survival centres in the brainstem, and coloured by the survival emotions paired or associated with the sensory stimuli being analyzed, including the physiological responses to these emotions, and is the basis of Conditioned Learning. These primary survival emotions may disrupt on-going sensory processing and integration at this and higher levels. Processing at this level is subconscious.

When survival emotions of the Fight or Flight response are activated above some “threshold” value, the amygdala and other brainstem structures such as the Periaqueductal Grey Matter of the midbrain inhibit frontal cortical processing, interfering with reasoning and problem-solving. The cause of this loss of higher level conscious cortical processing is a direct consequence of activation of the subconscious primary survival emotions of the Limbic System and Brainstem.

Secondary processing of the sensory stimuli in the Brainstem, Limbic System and lower cortical levels generates a series of control functions defining the nature of the sensory data stream (e.g. control of pupils in vision) and second-order integration of this sensory data (e.g. movement, shape and location of object in space). Processing at this level is subconscious.

Further processing in the palaecortical components of the Limbic System (e.g. hippocampus, cingulate, subcallosal and orbitofrontal cortices) generates secondary emotions relative to the sensory data stream and primary emotions already supplied by the amygdala and other brainstem areas via sampling memory of related events. These secondary limbic emotions may disrupt on-going sensory processing and integration at this and higher levels. Processing at this level is largely subconscious.

Initial cortical processing is predominately bilateral and subconscious, and is dependent upon earlier processing at brainstem and subcortical levels. Emotions, either primary or secondary, may disrupt on-going sensory processing and integration at this and higher levels.

At some level of cortical processing the sensory data stream emerges into a conscious perception, and is dependent upon earlier processing at brainstem, subcortical, and earlier cortical levels. Emotions, either primary or secondary, may disrupt on-going integration at this and higher levels

At the highest levels of cortical processing, the processing is largely done in one hemisphere or the other and perceived consciously as a logical, rational thought or a visuospatial Gestalt, and is dependent upon earlier processing at brainstem, subcortical and cortical levels. Emotions, either primary or secondary, may disrupt on-going integration at this level, and any “thinking” dependent upon this level of processing.

Thinking about the fully processed and integrated sensory experience in the frontal lobes, based upon remembered sensory experiences relevant to the current experience may lead to decisions, which will be represented neurologically by activation of either Logic or Gestalt “lead” functions or both.

These “lead” functions will then initiate a cascade of neurological flow, which is initially frontal cortical, but rapidly flows into other cortical areas and subcortical structures like the basal ganglia, thalamus, and cerebellum, which in turn feedback to the cortex and each other. Emotions, either primary or secondary, may disrupt on-going processing and integration at any level of this process, and thus overtly affect the final outcome of the cognitive functions taking place.

Coherent neurological processing at any stage of the above process is dependent upon both uninterrupted flows along integrative pathways and within integrative processing centres. Disruption or de-synchronisation of the timing of these integrative neural flows or disruption or de-synchronisation of processing in any of the integrative centres may result in loss of cognitive function.

Maintaining integration along all integrative pathways and within all integrative centres produces optimum function, a state called Brain Integration in LEAP.

Loss of integrated brain function is the principal cause of dysfunction in both mental and physical performance, called Loss of Brain Integration in LEAP.

The primary mechanism causing Loss of Brain Integration is de-synchronisation and loss of timing of neural flows along integrative pathways and within integrative centres by inhibition or excitation of these pathways and centres by neural flows originating from brainstem and limbic survival related emotions.

On-going Loss of Brain Integration is often generated by early childhood trauma that creates long-term disruption of Brain Integration as a mechanism of coping.

Other factors affecting Brain Integration are genetic, structural, organic brain damage, and environmental stressors:

o Structural defects or abnormalities can be of developmental origin, e.g. neuronal migration problems, or result from toxin exposure at specific critical periods of development, e.g. fetal alcohol syndrome. Many cognitive defects have been shown to correlate with abnormalities in brain structure.24

o Organic Brain Damage may result from a head injury, and this damage often results in sclerosis that disrupts neural flows underlying Brain Integration (e.g. hippocampal sclerosis and subsequent epilepsy are often associated with learning disorders).

o Genetic Factors affecting Brain Integration are often genes that code for specific alleles for specific enzymes involved in maintaining normal levels of neurotransmitters or receptors in brain circuits.25 Deficiencies in either neurotransmitters or receptors will compromise Brain Integration, and have behavioural consequences. This is both the basis of much ADHD behaviour and the justification for drug use to ameliorate these behaviours.26

Other genes may code for alleles that affect fatty acid metabolism and utilisation, especially in maintaining neuronal membrane stability and function. This affects predominately physical co-ordination and reading.27

o Diet and nutritional deficiencies may also compromise brain function and result in loss of Brain Integration. Diets rich in fast or junk foods often create marginal nutritional deficiencies that may disrupt brain function, and often contain various preservatives and additives, like the azo-food dye tartrazine, that may cause a total loss of brain integration in sensitive individuals28.

Indeed, the misbehaviour and academic performance of children and young adults have been shown to improve significantly with diet change or nutritional supplementation29, and several recent books have discussed this aspect of behaviour and learning problems30.

o Environmental factors such as electromagnetic fields emitted from man-made electronic equipment and Geopathic stress from distortions in the earth’s electromagnetic fields may affect the brain integration of sensitive individuals and result in learning problems. 31

Loss of Brain Integration and Compensation

When Brain Integration is lost via disruption of the most efficient neural pathways and/or centres, either by organic damage or by functional inhibition of cortical or subcortical functions due to outputs from survival centres in the brain, specific conscious functions dependent upon this integration is also disrupted. The overt loss of conscious function is, however, often far less than the degree of interference with underlying functions might suggest because the brain is a master at compensation and will automatically compensate for these disrupted flows by using other areas of the brain, both conscious and subconscious to produce the most efficient processing possible.

Thus, even children with considerable organic brain damage will often establish compensatory neurological patterns of activity to produce varying levels of function in spite of massive disruption of neural pathways underlying normal function, e.g. children with cerebral palsy may learn to walk and talk. It is indeed this tremendous compensatory capacity of the brain that allows even highly disintegrated brains to produce some degree of function, however, the level of dysfunction controls the degree of compensation. Thus, the greater the degree of dysfunction present, the lesscompensation that is possible.

If the disruption of integrated function is at the more basal levels of integration, the ability to compensate for the resulting dysfunction is much more limited than if the loss of integration is at a higher level of processing because all higher levels of processing are dependent upon the quality of the data integrated at earlier levels of processing. For instance, while damage to an early component of vision, say the retina or optic nerve totally disrupts sight, damage and hence loss of integration in the V3 area of the occipital cortex may leave the image fully intact, but disrupt only colour vision.

When the highest levels of cortical integration are disrupted directly or lower level cortical or subcortical functions underlying these higher cortical functions are disrupted, we may lose the capacity to “think” in certain ways. For instance, we may maintain Gestalt creative abilities (e.g. be good at art and design), but lose the ability to perform even simple mathematics because of the loss of the ability to abstract (e.g. are hopeless at maths). Specific Learning Disorders result from the loss of integration in of higher-level cortical functions or lower-level subconscious cortical or subcortical functions supporting these higher-level functions directly activated by consciousness.

Children and adults suffering Specific Learning Disorders usually know what they need to do, often even how to do it (e.g. I want to spell this word, so I need to sequence the letters and remember this sequence). But they just cannot activate the necessary subcortical and cortical processing to do what they know how and want to do consciously because of loss of integration at some level of neural processing required to do this function. When this loss of Brain Integration affects their ability to read, spell, write or do mathematics, it results in SLDs. However, they will still attempt to perform these functions, but in some compensated way. For instance, a child that cannot spell words correctly (that is, visually in English), still attempts to spell words, but using phonetics to compensate for the “mind’s eye” image he/she cannot create.

Because the level at which the integration is disrupted is unknown to the consciousness and compensation is largely subconscious and automatic, a person with Specific Learning Disorders is only aware that some function is difficult or not possible to perform, but not why this is so. Most often Brain Integration is lost in subconscious functions that were never accessible to our consciousness in the first place.

The Average Teenage Brain – Great Article!

Tuesday, July 26th, 2016

I found this fantastic article about the teenage brain – how tough is it being a parent these days? There’s more anxiety, depression, suicidal thoughts and damaging behaviours – our children are suffering.   Children respond so well to kinesiology – it helps to diffuse the stress patterns, naturopathically we can support better mood and hormone levels and energetically we can support keeping kids balanced.  Eventually teenage stress leads to adrenal exhaustion or immune dysfunction, creating challenges in their early adult years.

Luckily at New Leaf Natural Therapies there are many things we can do to help teenagers – treatments and nutrients.  Call us on 3348 6098 to discuss how we can help your child.

“During adolescence the brain’s ability to change is especially pronounced—and that can be a double-edged sword. Jay N. Giedd, a child and adolescent psychiatrist at the National Institute of Mental Health who specializes in brain imaging, points out that the brain’s plasticity allows adolescents to learn and adapt, which paves the way for independence. But it also poses dangers: different rates of development can lead to poor decision making, risk taking—and, in some cases, diagnosable disorders.

Across cultures and millennia, the teen years have been noted as a time of dramatic changes in body and behaviour. During this time most people successfully navigate the transition from depending upon family to becoming a self-sufficient adult member of the society. However, adolescence is also a time of increased conflicts with parents, mood volatility, risky behaviour and, for some, the emergence of psychopathology.

The physical changes associated with puberty are conspicuous and well described. The brain’s transformation is every bit as dramatic but, to the unaided eye, is visible only in terms of new and different behaviour. The teen brain is not broken or defective. Rather, it is wonderfully optimised to promote our success as a species.

Beginning in childhood and continuing through adolescence, dynamic processes drive brain development, creating the flexibility that allows the brain to refine itself, specialize and sharpen its functions for the specific demands of its environment. Maturing connections pave the way for increased communication among brain regions, enabling greater integration and complexity of thought. When what we call adolescence arrives, a changing balance between brain systems involved in emotion and regulating emotion spawns increased novelty seeking, risk taking and a shift toward peer-based interactions.

These behaviours, found in all social mammals, encourage separating from the comfort and safety of our families to explore new environments and seek unrelated mates.1 However, these potentially adaptive behaviours also pose substantial dangers, especially when mixed with modern temptations and easy access to potent substances of abuse, firearms and high-speed motor vehicles.

In many ways adolescence is the healthiest time of life. The immune system, resistance to cancer, tolerance for heat and cold and several other variables are at their peak. Despite physical strengths, however, illness and mortality increase 200 percent to 300 percent. As of 2005, the most recent year for which statistics are available, motor vehicle accidents, the No. 1 cause, accounted for about half of deaths. Nos. 2 and 3 were homicide and suicide.2 Understanding this healthy-body, risk-taking-brain paradox will require greater insight into how the brain changes during this period of life. Such enhanced understanding may help to guide interventions when illnesses emerge or to inform parenting or educational approaches to encourage healthy development.

Adolescent Neurobiology: Three Themes

The brain, the most protected organ of the body, has been particularly opaque to investigation of what occurs during adolescence. But now the picture emerging from the science of adolescent neurobiology highlights both the brain’s capacity to handle increasing cognitive complexity and an enormous potential for plasticity—the brain’s ongoing ability to change. The advent of structural and functional magnetic resonance imaging (MRI), which combines a powerful magnet, radio waves, and sophisticated computer technology to provide exquisitely accurate pictures of brain anatomy and physiology, has opened an unprecedented window into the biology of the brain, including how its tissues function and how particular mental or physical activities change blood flow. Because the technique does not use ionizing radiation, it is well suited for pediatric studies and has launched a new era of neuroscience. Three themes emerge from neuroimaging research in adolescents:

  1. Brain cells, their connections and receptors for chemical messengers called neurotransmitters peak during childhood, then decline in adolescence.
  2. Connectivity among brain regions increases.
  3. The balance among frontal (executive-control) and limbic (emotional) systems changes.

These themes appear again and again in our studies of the biological underpinnings for cognitive and behavioral changes in teenagers.

Theme 1: Childhood Peaks Followed by Adolescent Declines in Cells, Connections and Receptors

The brain’s 100 billion neurons and quadrillion synapses create a multitude of potential connection patterns. As teens interact with the unique challenges of their environment, these connections form and re-form, giving rise to specific behaviors—with positive or negative outcomes. This plasticity is the essence of adolescent neurobiology and underlies both the enormous learning potential and the vulnerability of the teen years.

Neuroimaging reveals that gray matter volumes—which reflect the size and number of branches of brain cells—increase during childhood, peak at different times depending on the location in the brain, decline through adolescence, level off during adulthood and then decline somewhat further in senescence. This pattern of childhood peaks followed by adolescent declines occurs not only in gray matter volumes but also in the number of synapses and the densities of neurotransmitter receptors.3 This one-two punch—overproduction followed by competitive elimination—drives complexity not only in brain development but also across myriad natural systems.

Theme 2: Increased Connectivity

Many cognitive advances during adolescence stem from faster communication in brain circuitry and increased integration of brain activity. To use a language metaphor, brain maturation is not so much a matter of adding new letters as it is one of combining existing letters into words, words into sentences and sentences into paragraphs.

“Connectivity” characterizes several neuroscience concepts. In anatomic studies connectivity can mean a physical link between areas of the brain that share common developmental trajectories. In studies of brain function, connectivity describes the relationship between different parts of the brain that activate together during a task. In genetic studies it refers to different regions that are influenced by the same genetic or environmental factors. All of these types of connectivity increase during adolescence.

In structural magnetic resonance imaging studies of brain anatomy, connectivity, as indicated by the volume of white matter—bundles of nerve cells’ axons, which link various regions or areas of the brain—increases throughout childhood and adolescence and continues to grow until women reach their 40s and men their 30s. The foundation of this increase in wiring is myelination, the formation of a fatty sheath of electrical insulation around axons, which speeds conduction of nerve impulses. The increase is not subtle—myelinated axons transmit impulses up to 100 times faster than unmyelinated axons. Myelination also accelerates the brain’s information processing via a decrease in the recovery time between firings. That allows up to a 30-fold increase in the frequency with which a given neuron can transmit information. This combination—the increase in speed and the decrease in recovery time—is roughly equivalent to a 3,000-fold increase in computer bandwidth.

However, recent investigations into white matter are revealing a much more nuanced role for myelin than a simple “pedal to the metal” increase in transmission speed. Neurons integrate information from other neurons by summing excitatory and inhibitory input. If excitatory input exceeds a certain threshold, the receiving neuron fires and initiates a series of molecular changes that strengthens the synapses, or connections, from the input neurons. Donald Hebb famously described this process in 1940 as “cells that fire together wire together.” It forms the basis for learning. In order for input from nearby and more distant neurons to arrive simultaneously, the transmission must be exquisitely timed. Myelin is intimately involved in the fine-tuning of this timing, which encodes the basis for thought, consciousness and meaning in the brain. The dynamic activity of myelination during adolescence reflects how much new wiring is occurring.

On the flip side, recent research reveals that myelination also helps close the windows of plasticity by inhibiting axon sprouting and the creation of new synapses.4 Thus, as myelination proceeds, circuitry that is used the most becomes faster, but at the cost of decreased plasticity.

Advances in imaging techniques such as diffusion tensor imaging (DTI) and magnetization transfer (MT) imaging have helped spark interest in these processes by allowing researchers to characterize the direction of axons and the microstructure of white matter. These new techniques further confirm an increase in white matter organization during adolescence, which correlates in specific brain regions with improvements in language,5 reading,6 ability to inhibit a response7 and memory.5

Functional magnetic resonance imaging studies also consistently demonstrate increasing and more efficient communication among brain regions during child and adolescent development. We can measure this communication by comparing regions’ activation during a task. In studies assessing memory8 and resistance to peer pressure,9 the efficiency of communication in the relevant circuitry was a better predictor of how teens performed than was a measurement of metabolic activity in the regions involved.

These lines of investigation, along with EEG studies indicating increased linking of electrical activity in different brain regions, converge to establish a fundamental maturation pattern in the brain: an increase in cognitive activity that relies on tying together and integrating information from multiple sources. These changes allow for greater complexity and depth of thought.

Theme 3: Changing Frontal/Limbic Balance

The relationship between earlier-maturing limbic system networks, which are the seat of emotion, and later-maturing frontal lobe networks, which help regulate emotion, is dynamic. Appreciating the interplay between limbic and cognitive systems is imperative for understanding decision making during adolescence. Psychological tests are usually conducted under conditions of “cold cognition”—hypothetical, low-emotion situations. However, real-world decision making often occurs under conditions of “hot cognition”—high arousal, with peer pressure and real consequences. Neuroimaging investigations continue to discern the different biological circuitry involved in hot and cold cognition and are beginning to map how the parts of the brain involved in decision making mature.

Frontal lobe circuitry mediates “executive functioning,” a term encompassing a broad array of abilities, including attention, response inhibition, regulation of emotion, organization and long-range planning. Structural MRI studies of cortical thickness indicate that areas involved in high-level integration of input from disparate parts of the brain mature particularly late and do not reach adult levels until the mid 20s

Across a wide variety of tasks, fMRI studies consistently show an increasing proportion of frontal versus striatal or limbic activity as we progress from childhood to adulthood. For example, among 37 study participants aged 7–29, the response to rewards in the nucleus accumbens (related to pleasure seeking) of adolescents was equivalent to that in adults, but activity in the adolescent orbitofrontal cortex (involved in motivation) was similar to that in children.11 The changing balance between frontal and limbic systems helps us understand many of the cognitive and behavioral changes of adolescence.

Normal Changes versus Pathology

One of the greatest challenges for parents and others who work with teens is to distinguish sometimes exasperating behavior from genuine pathology. Against the backdrop of healthy adolescence, which includes a wide range of mood fluctuations and occasional poor judgment, is the reality that many types of pathology emerge during adolescence, including anxiety disorders, bipolar disorder, depression, eating disorders, psychosis, and substance abuse. The relationship between normal neurobiological variations and the onset of psychopathology is complicated, but one underlying theme may be that “moving parts get broken.” In other words, development may go awry, predisposing adolescents to disorders. Although neuroimaging is beginning to establish correlations between brain structure or function and behavior, a link between typical behavioral variations and psychopathology has not been firmly established. For example, the neural circuitry underlying teen moodiness may not be the same circuitry involved in depression or bipolar disorder. A greater understanding of the relationship between specific adolescent brain changes and their specific cognitive, behavioral and emotional consequences may provide insight into prevention or treatment.

In the meantime, late maturation of the prefrontal cortex, which is essential in judgment, decision making and impulse control, has prominently entered discourse affecting the social, legislative, judicial, parenting and educational realms. Despite the temptation to trade the complexity and ambiguity of human behavior for the clarity and aesthetic beauty of colorful brain images, we must be careful not to over-interpret the neuroimaging findings as they relate to public policy. Age-of-consent questions are particularly enmeshed in political and social contexts. For example, currently in the United States a person must be at least 15 to 17 years old (depending on the state) to drive, at least 18 to vote, buy cigarettes, or be in the military, and at least 21 to drink alcohol. The minimum age for holding political office varies as well: some municipalities allow mayors as young as 16, and the minimum age for governors ranges from 18 to 30. (On the national level, 25 is the minimum age to be a member of the U.S. House of Representatives, and 35 to be a senator or the president.) The age to consent to sexual relations varies worldwide from puberty (with no specific age attached) to age 18. In most laws the age at which a female can consent to sexual relations is lower than the age for a male. In the United States the legal age to consent to sexual intercourse varies by state from 14 to 17 for females and from 15 to 18 for males. Clearly, these demarcations reflect strong societal influences and do not pinpoint a biological “age of maturation.” For instance, the age of majority was increased from 15 to 21 in 13th-century England because one needed both to be strong enough to bear the weight of protective armor and to acquire the necessary skills for combat. Societal influences also contributed to the 26th Amendment to the United States Constitution, which in 1971 lowered the voting age from 21 to 18 to address the discrepancy between being able to be drafted and being able to vote. Delineating the proper role of developmental neuroscience, particularly neuroimaging, in informing public policy on age-of-consent issues will require extensive deliberation with input from many disciplines.

From the perspective of evolutionary adaptation, it is not surprising that the brain is particularly changeable during adolescence—a time when we need to learn how to survive independently in whatever environment we find ourselves. Humans can survive in the frozen tundra of the North Pole or in the balmy tropics on the equator. With the aid of technologies that began as ideas from our brains, we can even survive in outer space. Ten thousand years ago, a blink of an eye in evolutionary time spans, our brains may have been optimized for hunting or for gathering berries. Now our brains may be fine-tuned for reading or programming computers. This incredible changeability, or plasticity, of the human brain is perhaps the most distinctive feature of our species. It makes adolescence a time of great risk and great opportunity.

 

References

1. L. P. Spear, “The Adolescent Brain and Age-Related Behavioral Manifestations,” Neuroscience and Biobehavioral Reviews 24, no. 4 (2000): 417.

2. Centers for Disease Control and Prevention Health Data Interactive, http://205.207.175.93/hdi/ReportFolders/ReportFolders.aspx?IF_ActivePath=P,21, Mortality by underlying and multiple cause, ages 18+: US, 1981-2005 (Source: NVSS); accessed February 23, 2009.

3. F. M. Benes, in C. A. Nelson and M. Luciana, eds., Handbook of Developmental Cognitive Neuroscience (Cambridge, MA: MIT Press, 2001), 79.

4. R. D. Fields, “White Matter in Learning, Cognition, and Psychiatric Disorders,” Trends in Neurosciences 31, no. 7 (2008): 361.

5. Z. Nagy, H. Westerberg, and T. Klingberg, “Maturation of White Matter Is Associated with the Development of Cognitive Functions during Childhood,” Journal of Cognitive Neuroscience 16, no. 7 (2004): 1227.

6. G. K. Deutsch, R. F. Dougherty, R. Bammer, W. T. Siok, J. D. E. Gabrieli1,  B. Wandell, “Children’s Reading Performance Is Correlated with White Matter Structure Measured by Diffusion Tensor Imaging,” Cortex 41, no. 3 (2005): 354.

7. C. Liston, R. Watts, N. Tottenham, M. C. Davidson, S. Niogi, A. M. U., B.J. Casey, “Frontostriatal Microstructure Modulates Efficient Recruitment of Cognitive Control,” Cerebral Cortex 16, no. 4 (2006): 553.

8. V. Menon and S. Crottaz-Herbette, “Combined EEG and fMRI Studies of Human Brain Function,” International Review of Neurobiology 66 (2005): 291.

9. M. H. Grosbras, M. Jansen, G. Leonard, A. McIntosh, K. Osswald, C. Poulsen, L. Steinberg, R. Toro, and T. Paus, “Neural Mechanisms of Resistance to Peer Influence in Early Adolescence,” Journal of Neuroscience 27, no. 30 (2007): 8040.

10. N. Gogtay, J. N. Giedd*, L. Lusk, K. M. Hayashi, D. Greenstein, A. C. Vaituzis, T. F. Nugent III, D. H. Herman, L. S. Clasen, A.r W. Toga, J. L. Rapoport, and P. M. Thompson, “Dynamic Mapping of Human Cortical Development during Childhood through Early Adulthood,” Proceedings of the National Academy of Sciences of the United States of America 101, no. 21 (2004): 8174.

11. J. M. Bjork, B. Knutson, G. W. Fong, D. M. Caggiano, S. M. Bennett, and D. W. Hommer, “Incentive-Elicited Brain Activation in Adolescents: Similarities and Differences from Young Adults,” Journal of Neuroscience 24, no. 8 (2004): 1793.