In aging and many disease states, the energy production capacity of the body’s cells is diminished. The mitochondria are the structures within the cell responsible for generating energy from oxygen and nutrients. If their number is reduced or their function is impaired, free radicals are produced and damaging toxins accumulate in the cells. These toxins further damage the mitochondria and impair other aspects of cellular function. Many of the most common health problems, such as obesity, diabetes, and many problems associated with aging, arise from problems in cellular energy production. As one group of researchers has put this, "[a]ging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan."¹ Another has observed, "[m]itochondrial biogenesis [the creation of new mitochondria] is a key physiological process that is required for normal growth and development and for maintenance of ongoing cellular energy requirements during aging."² These observations link two key aspects of mitochondrial health, preventing and removing damaged mitochondria (mitophagy) and creating new mitochondria (mitogenesis).

Although the importance of the mitochondria as a central point of health has been accepted for decades, over the last few years the understanding of the mechanisms involved has changed significantly. Twenty or ten years ago, antioxidants and the free radical theory of aging largely dominated thinking. Today, the importance of mitochondrial biology linking basic aspects of aging and the pathogenesis of age-related diseases remains strong, yet the emphasis has changed. The focus has moved to mitochondrial biogenesis and turnover, energy sensing, apoptosis, senescence, and calcium dynamics.³

What Promotes Mitochondrial Biogenesis?
The body maintains a complex network of sensors and signaling functions to maintain stability despite a constantly changing environment and numerous challenges. Of special note is the concept of hormesis, meaning a state in which mild stress leads to compensation that improves the ability of the body to respond in the future to similar challenges. It turns out that many of the approaches that are associated with longevity and healthy aging promote hormesis. In terms of mitochondria biogenesis, these include caloric restriction, certain nutrient restrictions or shortages, caloric restriction mimetics, and exercise.

Many of the mechanisms that activate mitochondrial biogenesis in the face of hormesis have been elucidated. Keeping in mind that there always must be a balance between the elimination of worn-out and defective mitochondria and the generation of new ones, the activators of both actions can overlap. For instance, low energy levels (caloric restriction) and increased reactive oxygen species/free radicals can promote the activity of special cellular control points. These include activating metabolic sensors such as AMP kinase/ AMPK (adenosine monophosphate kinase) and the protein known as SIRT1 (sirtuin 1, i.e., silent mating type information regulation 2 homolog 1). Activated AMPK is an indicator that cellular energy is low and serves as a trigger to increase energy production. It inhibits insulin/IGF-1/mTOR signaling, all of which are anabolic and can lead not just to tissue production, such as muscle growth, but also to fat storage. Along with SIRT1, AMPK activates the biogenesis of new mitochondria to enable the cell to generate more energy. At the same time, activated AMPK and SIRT1 increase the activity of a tumor suppressor that induces mitophagy. The balance of the dual activations replaces defective mitochondria with newly formed functionally competent mitochondria.

A key to health and healthy aging is to regulate the catabolic processes via controlled amounts and types of stressors such that worn out mitochondria are removed without overshooting the mark and reducing overall cellular and tissue functionality. The most successful way to maintain this balance is to follow the body’s own natural metabolic signals rather than to attempt to override the body’s checkpoints. AMPK and SIRT1 ultimately are energy/nutrient sensors or control points. Hence rather than attempting to manipulate these directly, it likely is safer and ultimately more effective to address the factors in the cell that these sensors sense. The recent attention in the issue of aging to the role of NAD+ (the oxidized form of nicotinamide adenine dinucleotide) is a good example of this principle. Directions coming from the nucleus of the cell that help to regulate the normal production of NAD+ and the ratio between distinct pools found in the cytoplasm and in the mitochondria decline with age. The changes in the NAD+ from the nucleus lead to a disruption on the mitochondrial side. In terms of energy production, it is a bit like losing a link or two in the timing chain on your car engine with a resultant reduction in engine efficiency. To date, attempts to increase NAD+ in cells via supplementation with precursors have not proven particularly successful. Major benefits have been demonstrated in animal models only in the already seriously metabolically impaired or the relatively old. Recent research on oral supplementation has led to at least one extremely difficult article which, at least in this author’s opinion, delivers more smoke than heat.4,5 There is, however, an argument to the effect that supplementing together both nicotinamide riboside (a NAD+ precursor) and a sirtuin activator, such as pterostilbene, may prove to be more successful.

It turns out that there are key points in normal cellular energy generation processes that strongly influence the NAD+ pools available for the cell to draw upon and the rate at which NAD+ can be replaced in these pools. Aging has been shown to promote the decline of nuclear and mitochondrial NAD+ levels and to increase the risk of cancer along with components of the metabolic syndrome. It is significant that the risks of these conditions can be reduced in tandem. Three places to start are 1) the pyruvate dehydrogenase complex, 2) the tricarboxylic acid cycle (TCA cycle) also known as the Krebs Cycle, and 3) the malate shuttle. A fourth junction is Complex I of the electron transport system, again, in the mitochondria.6 Manipulation of steps (1) and (2) already is being used in cancer treatment.7 Readily available dietary supplements can influence all four of these metabolic bottlenecks.

Supplements for Promoting Mitochondrial Biogenesis
Medicine has started to pay a great deal of attention to effecting mitochondrial biogenesis through not just drugs, but also dietary supplements. Those interested should go online and look up "Mitochondrial Biogenesis: Pharmacological Approaches" in Current Pharmaceutical Design, 2014, Vol. 20, No. 35. Quite a few options are mentioned, including well known compounds, such as R-lipoic acid (including with L-carnitine), quercetin and resveratrol, along with still obscure supplements, including various triterpenoids and the Indian herb Bacopa monnieri.

Pomegranate, French White Oak and Walnuts
The pomegranate, with its distinctive scarlet rind (pericarp) and vibrantly colored seed cases (arils), is one of the oldest cultivated fruits in the world. This exotic fruit features prominently in religious texts and mythological tales and has been revered through the ages for its medicinal properties. An image of a pomegranate even can be found on the shield of the British Royal College of Medicine. Numerous studies have demonstrated the benefits of the fruit for cardiovascular health with other benefits suggested in areas ranging from arthritis to stability of cell replication to bone health. Now a study in Nature Medicine (July 2016) has uncovered perhaps the most important benefit of all, the ability of pomegranate compounds (ellagitannins) transformed by gut bacteria to protect the mitochondria of the muscles and perhaps other tissues against the ravages of aging. The mitochondria are the energy generators of the cells and the weakening of this energy generating function in an increasing percentage of mitochondria as we age is a primary source of physical decline over the years. Urolithin A, a byproduct of gut bacterial action on pomegranate compounds, allows the body to recycle defective mitochondria and thereby slow or even reverse for a time some of the major aspects of aging. The lifespan in a nematode model of aging was increased by more than 45 percent. Older mice in a rodent model of aging exhibited 42 percent better exercise endurance. Younger mice also realized several significant benefits.⁸

Beginning almost three decades ago, there were numerous speculations in the research world regarding the so-called "French Paradox" in which the French consumed quite large amounts of saturated fat in the form of butter and cheese, yet consistently experienced much lower rates of cardiovascular disease than did Americans. Not only that, the French, especially in the southwest of the country, typically led longer lives even in the areas noted for consuming large amounts of goose fat and pate de foie gras, which is to say, not just the Mediterranean diet based on olive oil, etc. One hypothesis put forth very early on was that it was the French consumption of red wine that protected them. It was thought that red wine components, including anthocyanidins, proanthocyanidins and resveratrol, are the protective compounds. Not considered until recently is that French red wines traditionally have been aged in casks made from white oak (Quercus robur). White oak contains roburin A, a dimeric ellagitannin related chemically to punicalagin. Human data show relatively good absorption and conversion of roburins into substances including urolithin A and ellagic acid—as compared with ellagitannins in general, which evidence only poor absorption. Hence, the benefits of good red wine traditionally produced and good cognac (also aged in oak barrels) involve urolithin A. Notably, the benefits of roburins, most likely derived from the conversion to urolithin A, go beyond mitophagy to include ribosomes, referring to cell components that translate DNA instructions into specific cellular proteins.^9,10,11,12

Other sources of ellagitannins have been shown to lead to the production of urolithin A by bacteria in the human gut. Not surprisingly, sources of ellagitannins are foods long associated with good health longevity, including not just pomegranate and oak-aged red wine, but also walnuts (and a smattering of other nuts), strawberries, raspberries, blackberries, cloudberries and even black tea in small amounts.

Exercise and Pyrroloquinoline Quinone (PQQ)
Peroxisome proliferator-activated receptor gamma coactivator (PGC-1á) is the master regulator of mitochondrial biogenesis.¹³ Exercise is perhaps the most significant activator of PGC-1á that most individuals can access. Exercise, furthermore promotes mitochondrial biogenesis through a number of other pathways, especially endurance and interval training.¹⁴

There are non-exercise options. You can’t take PGC-1á orally because it is a large protein molecule which does not survive digestion. PQQ is a small molecule that is available when ingested and that increases circulating PGC-1á. PQQ supplementation leads to more mitochondria and more functional mitochondria.¹⁵

Fasting, Ketogenic Diets and Fasting-Mimicking Supplements As already discussed, fasting promotes mitochondrial biogenesis by AMPK activation.¹⁶ AMPK senses the energy status of the cell and responds both to acute shortages, such as that induced by exercise, and to chronic shortages, such as from fasting. Probably due to an overall reduction in metabolic rate, chronic caloric restriction (as opposed to intermittent fasting) contributes to the health of mitochondria rather than biogenesis.¹⁷ The robustness of AMPK response decreases with age.¹⁸

Ketogenic diets (very low carbohydrate diets) also promote increases in mitochondria.¹⁹ Few individuals are willing or able to follow ketogenic diets chronically just as few individuals are willing to undergo routine fasts. Fasting-mimicking supplements offer an alternative approach. The dietary supplement (-)–hydroxycitric acid (HCA) is the best researched of these compounds. (Keep in mind that there is a vast difference in the efficacy of commercially available forms.²⁰) Researchers have proposed that HCA used properly can activate mitochondrial uncoupling proteins and related effects.²¹

Furthermore, according to a study published in the journal Free Radical Research in 2014, HCA improves antioxidant status and mitochondrial function plus reduces inflammation in fat cells.²² Inflammation is linked to the metabolic syndrome at the cellular level by way of damage to the antioxidant enzyme system (e.g., superoxide dismutase, glutathione peroxidase, glutathione reductase) and mitochondria. This damage, in turn, propagates further production of pro-inflammatory mediators (e.g., TNF-á, MCP-1, IFN-ã, IL-10, IL-6, IL-1â). HCA protected fat cells from ER stress by improving the antioxidant status to reduce oxidative stress (i.e., reduce ROS) and improve the function of the mitochondria to short circuit an ER stress—inflammation loop in these cells. Reducing TNF-á is important in that doing so removes a major impediment to mitochondrial biogenesis.²³

Other Supplements to Promote Mitochondrial Biogenesis

Scholarly reviews looking at natural compounds such as those that are found in anti-aging diets suggest yet other supplements to promote mitobiogenesis. For instance, it turns out that hydroxytyrosol, the most potent and abundant antioxidant polyphenol in olives and virgin olive oil, is a potent activator of AMPK and an effective nutrient for stimulating mitochondrial biogenesis and function via what is known as the PGC-1á pathway.²⁴ Another herb with anti-aging effect, this time by activating the malate shuttle mechanism mentioned above, is rock lotus (Shi Lian Hua). This herb has been described in detail in this magazine in the article, "Uncovering the Longevity Secrets of the ROCK LOTUS."²⁵

Conclusion
It is possible to improve the functional capacity of the mitochondria through dietary practices, exercise and supplements. Indeed, a number of compounds have been identified by researchers as mitochondrial nutrients. These compounds work together to increase the efficiency of energy production, to reduce the generation of free radicals, and so forth and so on. Likewise, these nutrients have been shown to improve the age-associated decline of memory, improve mitochondrial structure and function, inhibit the ageassociated increase of oxidative damage, elevate the levels of antioxidants, and restore the activity of key enzymes. Perhaps best of all, the body can be encouraged both to remove damaged mitochondria (mitophagy) and to create new ones, which is to say, mitochondrial biogenesis.

References:

1. López-Lluch G, Irusta PM, Navas P, de Cabo R. Mitochondrial biogenesis and healthy aging. Exp Gerontol. 2008 Sep;43(9):813–9.
2. Stefano GB, Kim C, Mantione K, Casares F, Kream RM. Targeting mitochondrial biogenesis for promoting health. Med Sci Monit. 2012 Mar;18(3):SC1-
3. Gonzalez-Freire M, de Cabo R, Bernier M, Sollott SJ, Fabbri E, Navas P, Ferrucci L. Reconsidering the Role of Mitochondria in Aging. J Gerontol A Biol Sci Med Sci. 2015 Nov;70(11):1334-42.
4. Trammell SA, Schmidt MS, Weidemann BJ, Redpath P, Jaksch F, Dellinger RW, Li Z, Abel ED, Migaud ME, Brenner C. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun. 2016 Oct 10;7:12948.
5. Mitteldorf J. Nicotinamide Riboside —Where’s the Beef? http://joshmitteldorf.scienceblog.com/2014/11/17/nicotinamide-riboside-wheres-thebeef/.
6. Yang Y, Sauve AA. NAD+ metabolism: Bioenergetics, signaling and manipulation for therapy. Biochim Biophys Acta. 2016 Dec;1864(12):1787– 1800.
7. Schwartz L, Buhler L, Icard P, Lincet H, Steyaert JM. Metabolic treatment of cancer: intermediate results of a prospective case series. Anticancer Res.2014 Feb;34(2):973–80.
8. Ryu D, Mouchiroud L, Andreux PA, Katsyuba E, Moullan N, Nicolet-Dit-Félix AA, Williams EG, Jha P, Lo Sasso G, Huzard D, Aebischer P, Sandi C, Rinsch C, Auwerx J. Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nat Med.2016 Aug;22(8):879-88.
9. Pellegrini L, Belcaro G, Dugall M, Corsi M, Luzzi R, Hosoi M. Supplementary management of functional, temporary alcoholic hepatic damage with Robuvit® (French oak wood extract). Minerva Gastroenterol Dietol. 2016 Sep;62(3):245–52.
10. Vinciguerra MG, Belcaro G, Cacchio M. Robuvit® and endurance in triathlon: improvements in training performance, recovery and oxidative stress. Minerva Cardioangiol. 2015 Oct;63(5):403–9.
11. Országhová Z, Waczulíková I, Burki C, Rohdewald P, Ïuraèková Z. An Effect of Oak-Wood Extract (Robuvit®) on Energy State of Healthy Adults-A Pilot Study. Phytother Res. 2015 Aug;29(8):1219–24.
12. Natella F, Leoni G, Maldini M, Natarelli L, Comitato R, Schonlau F, Virgili F, Canali R. Absorption, metabolism, and effects at transcriptome level of a standardized French oak wood extract, Robuvit, in healthy volunteers: pilot study. J Agric Food Chem. 2014 Jan 15;62(2):443–53.
13. Ventura-Clapier R, Garnier A, Veksler V. Transcriptional control of mitochondrial biogenesis: the central role of PGC-1alpha. Cardiovasc Res. 2008 Jul 15;79(2):208–17.
14. Wright DC, Han DH, Garcia-Roves PM, Geiger PC, Jones TE, Holloszy JO. Exercise-induced mitochondrial biogenesis begins before the increase in muscle PGC-1alpha expression. J Biol Chem. 2007 Jan 5;282(1):194–9.
15. Bauerly K, Harris C, Chowanadisai W, Graham J, Havel PJ, Tchaparian E, Satre M, Karliner JS, Rucker RB. Altering pyrroloquinoline quinone nutritional status modulates mitochondrial, lipid, and energy metabolism in rats. PLoS One.2011;6(7):e21779.
16. Zong H, Ren JM, Young LH, Pypaert M, Mu J, Birnbaum MJ, Shulman GI. AMP kinase is required for mitochondrial biogenesis in skeletal muscle in response to chronic energy deprivation. Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):15983–7.
17. Lee CM, Aspnes LE, Chung SS, Weindruch R, Aiken JM. Influences of caloric restriction on age-associated skeletal muscle fiber characteristics and mitochondrial changes in rats and mice. Ann N Y Acad Sci. 1998 Nov 20;854:182–91.
18. Jornayvaz FR, Shulman GI. Regulation of mitochondrial biogenesis. Essays Biochem. 2010;47:69–84.
19. Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet. Epilepsia. 2007 Jan;48(1):43–58.
20. Louter-van de Haar J, Wielinga PY, Scheurink AJ, Nieuwenhuizen AG. Comparison of the effects of three different (-)-hydroxycitric acid preparations on food intake in rats. Nutr Metab(Lond). 2005 Sep 13;2:23.
21. McCarty MF. High mitochondrial redox potential may promote induction and activation of UCP2 in hepatocytes during hepatothermic therapy. Med Hypotheses.2005;64(6):1216–9.
22. Nisha VM, Priyanka A, Anusree SS, Raghu KG. (-)–Hydroxycitric acid attenuates endoplasmic reticulum stress-mediated alterations in 3T3-L1 adipocytes by protecting mitochondria and downregulating inflammatory markers. Free Radic Res.2014 Nov;48(11):1386-96.
23. Valerio A, Cardile A, Cozzi V, Bracale R, Tedesco L, Pisconti A, Palomba L, Cantoni O, Clementi E, Moncada S, Carruba MO, Nisoli E. TNFalpha downregulates eNOS expression and mitochondrial biogenesis in fat and muscle of obese rodents. J Clin Invest. 2006 Oct;116(10):2791–8.
24. Liu J, Shen W, Zhao B, Wang Y, Wertz K, Weber P, Zhang P. Targeting mitochondrial biogenesis for preventing and treating insulin resistance in diabetes and obesity: Hope from natural mitochondrial nutrients. Adv Drug Deliv Rev. 2009 Nov 30;61(14):1343–52.
25. http://www.totalhealthmagazine.com/Anti-Aging/Uncovering-the-Longevity-Secrets-of-the-ROCK-LOTUS.html.

• How a concussion or more properly termed, traumatic brain injury (TBI), affects your brain
• Your body’s natural defense against TBI
• How CBD reinforces this defense and can help heal TBI

What is TBI?
We’re hearing a lot more about traumatic brain injury in recent years, with increasing diagnoses among many prominent figures from military combat veterans to figures in such high impact sports as football and boxing. There has also been attention focused on child and teen sports, where the injuries can be even more damaging to their more vulnerable bodies. Fortunately, TBI is being taken a lot more seriously now than ever before.

In TBI, the head is impacted by an external force that causes the brain to swell within the confines of the skull, thus decreasing blood flow, and causing other chemical changes that adversely affect brain function. In many instances, the brain fully recovers. Far too often, however, patients are left with lasting issues such as memory problems, depression, motor impairment, anxiety, migraines, vision problems, trouble processing, and much more.

Standard Medical Treatment of TBI
The biomedical standard of care for TBI consists of these doctor’s orders:

• Rest in a dark room
• Don’t spend time in front of screens
• Lay off the books, the job, the studying
• Don’t do excessive thinking

This, in addition to surgery and occupational therapy for more severe cases, is about all doctors have to offer those with a traumatic brain injury, commonly referred to as concussion. Then, it’s a game of watch and wait. The brain is left to heal largely without any specific therapies to support the body’s natural healing processes.

Functional Medical Treatment of TBI
In contrast, those of us who use an integrative or functional medicine approach which focuses on treating underlying issues, have found that there is a better way to treat TBI. There are a number of anti-inflammatory herbs, such as curcumin, that help heal the brain. There are modalities, like hyperbaric oxygen (HBOT), which rescue brain cells by enhancing the flow of blood and oxygen. Then there is neurofeedback to train the brain in forming new pathways. Add in acupuncture, an ancient but still powerful treatment for TBI. All these treatments already take us beyond the mainstream standard of care.

A treatment that is (too slowly) gaining more mainstream acceptance are orally administered omega-3 fatty acids that reduce the inflammation and thus, lessen the swelling in the brain. You can read more about this in When Brain Collide, written by my colleague, Dr. Michael Lewis. His omega protocol, in which patients take a mega-dose of fish oil over the course of a few weeks, has had remarkable results. It has restored brain function in many including bringing people out of coma. Some years ago, my friend JJ Virgin’s son, Grant, had a devastating head injury, and I saw personally how high doses of fish oil was instrumental in bringing him back. This was even covered by Dr. Sanjay Gupta on a special on the topic for CNN.

CBD for TBI
Now we have a new modality: the administration of CBD for brain repair. Like many of us, Dr. Lewis is not only enthusiastic about its use, but fortunately is using his platform as a recognized TBI expert to educate the public and doctors alike about the benefits of adding CBD to the protocol.

The proof? Animal studies have demonstrated that cannabinoids can not only reduce the acute effects of TBI, mitigating neurological damage, but can also help with the secondary effects, including those frustrating cognitive deficits that can linger after even after a “minor” TBI.

The Science
CBD takes us from “There’s nothing we can do,” to “We definitely can help you!” How does this happen? Here is some of the science behind the phenomenon.

First of all, as mentioned, TBI causes the brain to swell and induce a potentially toxic level of activity of the excitatory neurotransmitter, glutamate. This can lead to varying amounts of cell death in significant portions of the brain. Inflammatory compounds and free radicals are also released, creating oxidative stress. These acute effects of TBI can lead to a host of secondary effects, potentially killing off more brain cells, weakening the blood brain barrier, and contributing some of the hallmark symptoms of TBI like brain fog, mood disruption, and sleep problems.

In my blog on the endocannabinoid system, you know that the ECS, the bodily system controlled by cannabinoids, is responsible for relaxing your body and returning it to balance in times of stress. It is also your body’s natural defense against TBI.

The ECS has two main receptors: CB1 and CB2. When activated, CB1 decreases excitatory glutamate activity. Excessive glutamate is toxic to brain cells, and the ECS has evolved to fight against it.

CB2, on the other hand, when activated revs up the immune response. It helps repair cells and promotes the creation of new neurons. This directly combats brain damage caused by cell death. Notably, CBD also preserves memory by preventing neuronal loss in the hippocampus, the brain’s memory center.

Brain Damaged Mice and CBD
In one study, researchers inflicted a TBI on mice genetically engineered to lack either CB1 or CB2 receptors. Their injuries were more severe compared to those of mice that had both receptors. Moreover, studies have shown that after a TBI, ECS activity increases to enact healing.

Another study showed that after a head injury was inflicted on a group of mice; when half of them were untreated and the other half received a single dose of plant derived endocannabinoid called 2-AG, there was a definite difference in outcome. The mice who received treatment improved in cognitive function, motor function and every parameter examined, even months later—a remarkable success. Of course, in a lab setting the scientists had the advantage of being able to administer the dose of 2-AG shortly after brain injury, so while it proved the point, it may be harder to do this in everyday head injuries.

CBD works best if administered in the “window of opportunity,” the critical moments after a brain injury, in which intervention can actually prevent brain damage. Typically, this window is a matter of minutes, 10 minutes, maybe an hour. CBD widens this window of opportunity. It works best up to 12 hours after an injury.

However, even if you had a brain injury, months or even years ago, CBD can still help by reducing brain inflammation and treating the secondary effects mentioned above, just not as well as if treated at the time. As long as you have symptoms from a TBI, CBD can have a positive effect.

How does it work?
CBD is what’s called a “promiscuous compound,” i.e., a chemical that binds to a variety of different receptors. That means CBD not only binds to the receptors of the ECS, but other receptors such as the serotonin receptor 5-HT1A and the PPAR-gamma nuclear receptor. These two receptors, when activated, protect the essential blood brain barrier which can be damaged during TBI. The blood brain barrier is a network of blood vessels and cells meant to keep unwanted substances out of the brain. It’s exceedingly difficult to pass through, and any weakening of it can allow otherwise unwanted substances to enter the brain. This can lead to inflammation and other brain conditions.

Serotonin, as you may know, is a major regulator of mood, and is the purported target of popular antidepressant medications, the SSRIs. CBD is known to boost mood not only through its impact on serotonin, but also dopamine, the pleasure or “reward” neurotransmitter, and GABA, the calming neurotransmitter. Thus, CBD can ease the depression and anxiety that can be so troublesome for those recovering from TBI.

More Brain Benefits
And it doesn’t stop with mood. CBD can also improve memory and lift brain fog. As mentioned, CBD can promote neuron growth in the hippocampus. It also regulates acetylcholine, which boosts memory and mental acuity.

One more huge benefit is the effect of CBD on PTSD (Post Traumatic Stress Disorder). It acts in the area of the limbic system, the seat of emotions, to help “forget” the fearful emotions associated with the traumatic event. This is important since PTSD is difficult to treat successfully by conventional means. There are specific trauma treatments such as EMDR, somatic experience, tapping and more, and they all work well, but even better in conjunction with CBD.

With all of its healing ability, CBD has yet become a standard treatment for brain injury. We hope that with more studies on its use, and simply, more experience by the public and the medical profession, it will become better accepted.

Luckily, you don’t have to wait for researchers to construct the perfect clinical trial in order to start using CBD.

Choose a full spectrum hemp oil extract which delivers the remedy as nature intended, with other cannabinoids and terpenes, so you get the best effect possible, known as the “entourage effect.”

How to Take CBD
Start out with a small dose and increase gradually, using your own response as a guide. Typical doses are 25–100 mg daily in divided doses 1–3 times daily. Doses are quite individual, based on your unique ECS activity.

Interactions with medications:
Even though CBD has a good safety profile, if you are taking medication, you should check with your doctor before trying it. Both CBD and most pharmaceuticals are detoxified by the liver’s cytochrome P450 enzyme system. As a result, certain medications, including chemotherapy agents, anti-epilepsy drugs, and the blood thinner coumadin may be affected. In some cases, you just have to have the drug dose decreased. For a list of potential drugs that may interact with CBD, see this link: https://cbdorigin.com/cbd-drug-interactions/ The fact is, though, we have found that doses under 100 mg a day generally do not interfere with medications.

Adjunctive Care
In addition to taking CBD, take large doses of omega-3 oils. I also agree with the conventional wisdom to rest your brain until medically cleared to become more active. You can enhance this rest with meditation and breathing exercises as well as good nutrition. Steer clear of all processed foods and sugar, and eat a plant-based diet that is also high in healthy omega-3 fats in such foods as avocados and wild caught (or sustainably raised farmed) salmon.

Other integrative supportive measures include neurofeedback, low level laser, PEMF, hyperbaric oxygen, Transcranial Magnetic Stimulation (TMS), and acupuncture. The bottom line here is that while we still have a lot to learn, there are increasing resources for treating this serious condition. Most exciting right now is the promise of CBD or more properly, Full Spectrum Hemp Oil Extract for treating TBI.

Abundant energy is the thing that truly defines youth. When we are young, our bodies have a tremendous ability to maintain the repair process. In science, we call this anabolic metabolism or having the ability to repair our cells faster then they are broken down. Anabolic metabolism also creates an effective fat burning and muscle enhancing atmosphere. In other words, instead of merely living, we feel truly alive.

In this day and age, we tend to break our bodies down faster than we can repair them-a process referred to as catabolic metabolism. Part of the reason for this is we are constantly in search of the elusive energy kick and we all too often try to find it by consuming copious amounts of caffeine, ephedrine, energy drinks or high energy bars. All of these stimulants provoke a temporary excitatory response from the body, but in the end, they take more from the body than they give. Unfortunately, this is often experienced as the energy crash.

Instead of finding ways to temporarily lift your energy levels and eventually come crashing to a screeching halt, what if you could provide each of your bodies cells with the nutrients they required to keep energy production at peak capacity? Would you be interested? Of course, you would, after all, who couldn't use a little more energy? Following are what I call the "energy trio"-carnitine, coenzyme Q-10 (Co-Q10) and alpha-lipoic acid (ALA), and if you use these three power nutrients properly, you may once again experience the energy potential you still have inside you.

In order to understand the importance of these three nutrients, let's first take a brief look at how your body produces energy. Inside the majority of your trillions of cells lies numerous little energy plants called mitochondria. These tiny little energy factories are responsible for producing at least 90 percent of the energy-carrying substance adenosine triphosphate (ATP).¹ Therefore, the vast majority of your energy is dependant upon how well your mitochondria are functioning.

Here's how the energy trio maintain abundant energy:

Fatty acids are the primary fuel source for ATP production; however, they are not able to cross the mitochondrial membrane without help. This help comes in the form of the natural vitamin-like substance L-carnitine, which acts as an energy transporter by shuttling fatty acids directly into the mitochondria to be burned as energy.² According to a 2004 study appearing in the journal Metabolism, healthy adults can greatly enhance their fat-burning ability by supplementing with L-carnitine.³

Recommended dosage: 500mg-2 grams.

Although mostly known for its cardiovascular benefits, Co-Q10 is essential to creating the spark that ignites fatty acid oxidation (burning).⁴ Aside from this roll, Co-Q10 also acts as a powerful antioxidant inside the mitochondria (where the majority of free radicals are formed).⁵

Recommended dosage: 30mg-150mg

Aside from being one of the most powerful and versatile of the antioxidants, ALA helps to increase overall ATP levels, thus enhancing energy levels.⁶ Research from the Linus Pauling Institute indicates that ALA in association with carnitine can greatly increase energy production and reverse the negative energy decline associated with aging in rodent models.⁷

Recommended dosage: 50mg-300mg

1. Crayhon, R., The Carnitine Miracle. M. Evans and Company, Inc. 1998
2. Fritz IB, Yue KTN. Long-chain carnitine acyltransferase and the role of acylcarnitine derivatives in the catalytic increase of fatty acid oxidation induced by carnitine. J Lipid Res 1963; 4:279-88.
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7. Hagen TM. Feeding acetyl-L-carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress. Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):1870-5.