Tuesday, January 28, 2014

Hemp going legit; some wonder if pot is far behind

Hemp going legit in federal farm bill agreement, some wonder if marijuana is far behind

Associated Press
Hemp going legit; some wonder if pot is far behind
In this Oct. 5, 2013 file photo, hemp chef Derek Cross helps harvest hemp during the first known harvest of the plant in more than 60 years, in Springfield, Colo. The federal farm bill agreement reached Monday Jan. 27, 2014 reverses decades of prohibition for hemp cultivation. Instead of requiring approval from federal drug authorities to cultivate the plant, the 10 states that have authorized hemp would be allowed to grow it in pilot projects or at colleges and universities for research. (AP Photo/Kristen Wyatt, Associated Press)

DENVER (AP) -- The federal government is ready to let farmers grow cannabis — at least the kind that can't get people high.
Hemp — marijuana's non-intoxicating cousin that's used to make everything from clothing to cooking oil — could soon be cultivated in 10 states under a federal farm bill agreement reached late Monday.
Some wonder if the move is an indication that the federal government is ready to follow the 20 states that have already legalized medical marijuana, including two that also allow its recreational use.
"This is part of an overall look at cannabis policy, no doubt," said Eric Steenstra, president of Vote Hemp, a Washington-based advocacy group.
However, opponents of legalized pot insist the hemp change doesn't mean marijuana is right behind.
Kevin Sabet, director of Smart Approaches to Marijuana, a national alliance that opposes legalization and imprisoning people for marijuana possession, downplayed the change to the farm bill.
"On the one hand, I think it's part of a larger agenda to normalize marijuana, by a few," Sabet said. "On the other hand, will it have any difference at the end of the day? I would be highly skeptical of that."
Hemp and marijuana are the same species, Cannabis sativa. Hemp, however, is cultivated to reduce or eliminate THC, marijuana's psychoactive chemical.
With the move allowing the cultivation of hemp, the U.S. government hopes to clear the way for farmers to compete in an industry currently dominated by China and Canada.
Even though it's not grown here, the U.S. is one of the fastest-growing hemp markets. In 2011, the U.S. imported $11.5 million worth of hemp products, up from $1.4 million in 2000. Most of that growth was seen in hemp seed and hemp oil, which finds its way into granola bars and other products.
Hemp has historically been used for rope but has hundreds of other uses: clothing and mulch from the fiber, foods such as hemp milk and cooking oil from the seeds, and creams, soap and lotions.
The 1970 Controlled Substances Act required farmers to get a permit from the Drug Enforcement Administration to grow hemp, though finished hemp products remained legal in the country. The last DEA hemp permit was issued in 1999 for a quarter-acre experimental plot in Hawaii. That permit expired in 2003.
The U.S. Department of Agriculture last recorded an industrial hemp crop in the late 1950s, down from a 1943 peak of more than 150 million pounds on 146,200 harvested acres.
Cultivation of the plant had congressional allies from both ends of the political spectrum. Democrats from marijuana-friendly states have pushed to legalize hemp cultivation, as have Republicans from states where the fibrous plant could be a profitable new crop.
"We are laying the groundwork for a new commodity market for Kentucky farmers," Sen. Mitch McConnell, R-Kentucky, said in a statement. McConnell was a lead negotiator on the inclusion of hemp in the farm bill.
The full House and Senate still must agree on the bill that will head to the House floor Wednesday.
Analysts have predicted legal hemp will remain a boutique crop, and the Congressional Research Service recently cited wildly differing projections about its economic potential.
Still, farmers interested in hemp say the farm bill agreement is a giant leap toward a viable hemp industry in this country.
However, Tom McClain, a Colorado hemp activist who helps connect nascent growers with buyers, said the industry won't get off the ground without more research.
"We don't have a compendium of information to go to," McClain said. "We do rely on universities and agricultural research to help us and direct us. We need local research to help drive the correct varieties, so that farmers get the best yield."
Ten states already allow the growing of hemp, though federal drug law has blocked actual cultivation in most. Those states are Colorado, Washington, California, Kentucky, Maine, Montana, North Dakota, Oregon, Vermont and West Virginia.
Earlier this month, the Colorado Department of Agriculture released licensing procedures for farmers interested in raising hemp.
About a dozen farmers didn't wait for the state rules and harvested small amounts last year — the nation's first acknowledged hemp crop in more than five decades. No statewide harvest totals were available.
Kristen Wyatt can be reached at http://www.twitter.com/APkristenwyatt
Hemp portion of the farm bill: http://bit.ly/1ncOCME

Friday, January 17, 2014

Hemp Healthy Information on Hemp Oil

Guide to Hemp Seed Oil


Why Hemp Oil?

Hemp oil, or hemp oil, is a tasty oil with a green or golden colour crushed from the seeds of the hemp plant (Cannabis sativa L.).
Traditionally used for food and body care, but almost forgotten, it is now making a strong comeback. It increasingly appears in the cold storage of health food markets as well as an ingredient in “natural” cosmetics.
Why? There are four main reasons:
•Hemp oil provides our body with a range of necessary nutrients and helps prevent a variety of common diseases. Particularly, its attractive fatty acid composition, i.e. its very high content of essential fatty acids, provides nutritional advantages over other vegetable oils.
•Carefully produced and stored hemp oil simply tastes good. Thus, instead of just being a food supplement, it can serve as a staple food in the modern kitchen.
•If used in cosmetics, it protects the skin and slows down its unavoidable aging process.
•Since hemp is usually grown in an eco-friendly manner, hemp oil is a truly natural product.
If used for cooking, cold pressed unrefined hemp oil lends its nutty flavour and healthy composition to a variety of foods. It is a delicious alternative wherever olive oil, walnut oil, or butter are used. Favourite hemp oil recipes include salad dressings, lightly stir fried or sautéed meats and vegetables, marinated vegetables and sauces. Or just try dipping bread into it.
Hemp oil has its limitations in cooking applications. Like other unrefined oils, hemp oil tends to smoke at relatively low temperatures. This indicates the formation of unhealthy oxidation and polymerization products and suggests that unrefined hemp oil should not be used for frying or deep-frying. This brochure takes a closer look at the nature, health benefits and various uses of hemp oil.

Some Oil Chemistry

A bit of knowledge on hemp oil’s composition will go a long way towards understanding its unique benefits. As with other vegetable oils, its main constituents are the so called fatty acids.
Despite the often confusing debate of “Fat: good or bad?” consumers have caught on to the idea that improper fat intake contributes to a host of – often fatal – illnesses. They’ve also heard that fats are “the more unsaturated the better”. The following sheds some, hopefully not too technical, light on the connection between fat composition and health.

Fatty Acids

Fats and oils have the same chemical structure but a different melting point: fats are solid at room temperature, oils are liquid. Chemically they are composed of a glycerol backbone with three fatty acids (FAs) attached. Each type of oil has a characteristic fatty acid composition (see Table below). Fatty acids are distinguished by their chain length, i.e. the number of carbon atoms, but most important is the distinction between saturated and unsaturated fatty acids.
Saturated fatty acids (SaFAs) are straight molecules. All carbon atoms are bonded the same way and with maximum strength. The parallel molecules stick easily to one another and fats high in SaFAs (e.g. animal lards, coconut fat) are solid a room temperature. The human body uses SaFAs primarily for energy storage. Until a few years ago, fats and oils with a high SaFA content had been preferred for foods because their saturated bonds are stable, resist oxidation and thus rancidity.
They can be used for frying, and are inexpensive. On the downside, it was discovered that the “sticky” SaFAs contribute strongly to the formation of clots and deposits in our blood vessels, to strokes and other common cardiovascular diseases. The recognition that “too much unsaturated fats kill too many people” has brought about a shift in food producers’ and consumers’ preference to oil containing more of the so-called
Unsaturated fatty acids (UFAs). They contain one (monounsaturated) or several (polyunsaturated) double bonds between adjacent carbon atoms. The resulting curved shape makes oils with a high UFA-content “slicker” and keeps them liquid down to lower temperatures. UFAs are the raw material for the construction of cell membranes and contribute to cell membrane fluidity. A diet low in UFAs forces the body to use SaFAs for the construction of cell membranes, resulting in cells with stiff, rigid membranes. UFAs also are needed as raw materials for many important messenger and regulator substances in our body (prostaglandins, hormones, neurotransmitters). There are many different UFAs produced in nature, primarily found in plant seeds but also in fish oil. Particularly important for the human diet are two of these UFAs, also referred to as;

Essential Fatty Acids

These two essential fatty acids (EFAs) are linoleic acid (LA) and alpha-linolenic acid (ALA). They are necessary for cell and body growth, maintenance of cell membranes, and as precursors to a variety of physiologically active regulators. They are called “essential” because our body cannot, as with other FAs, produce them ourselves. Instead, they must be present in our diet.
Linoleic acid is a double unsaturated fatty acid common in plants: Evening primrose oil contains up to 70% of its total fatty acid content as linoleic acid. Unrefined sun flower oil contains up to 65%, hemp oil up to 60%, soybean oil up to 55%, and flax oil up to 30% linoleic acid. The human body synthesizes another important fatty acid from linoleic acid: gamma-linolenic acid (see below).
Alpha-linolenic acid, a triple unsaturated fatty acid, is found in algae, crustaceans, and in fish oil. Only a few seeds of higher plants have substantial contents of this essential fatty acid: flax (up to 58%), hemp (up to 25%), canola and soybean (up to 12%).
In order to provide our body with sufficient, yet not too much EFAs, a nutritionally balanced diet should contain EFAs in a ratio of roughly 3:2 (linoleic acid: alpha-linolenic acid).
The distribution of essential fatty acids in hemp oil is close to this favourable ratio (2:1 to 3:1). Thus, if hemp oil is our only source of fatty acids, roughly two to four teaspoons per day suffice to meet our EFA needs. Flax oil, with its higher total EFA content has a much less favourable ratio of below 1:2.
i.e. contains very high proportions of ALA. Thus, it is suitable as a supplement in case of ALA deficiency, but not as everyday food oil.
Typical fatty acid composition of unrefined edible oils.

Fatty Acid
% of total oil
Acid *
gamma-Linolenic Acid (GLA)poly-unsaturated
In addition to alpha-linolenic acid, hemp oil contains typically 1-4% gamma-linolenic acid (GLA, C18:3w6) (from Erasmus 1994, Deferne&Pate 1996)

Gamma-Linolenic Acid (GLA)

In addition to the two EFAs, hemp oil is a source of yet another important polyunsaturated fatty acid, gamma-linolenic acid (GLA). In fact, it is the only edible oil with a relevant GLA content, typically 1-4%. Other GLA sources are evening primrose (6-14%) and borage (25-40%) oil. Because of their unattractive taste these oils are offered as dietary supplements, not as cooking oils.
As already mentioned, our diet usually contains sufficient linoleic acid, which our bodies convert enzymatically into GLA. Yet, in many people this conversion process is too slow for several reasons (high meat and fat diets, alcohol, genetic causes). This can result in decreased GLA levels and contribute to a number of common illnesses (see below). Supplementation of GLA with the diet can alleviate the resulting health problems.

Other Constituents

In addition to fatty acids, cold pressed hemp oil provides low to moderate quantities of other beneficial nutrients, for example: other rarely occurring polyunsaturated fatty acids, Tocopherols (Vitamin E), phytosterols and flavour compounds. Their amounts vary strongly with the hemp variety and the type of processing of the oil. The presence of these compounds in hemp oil also contributes to its reputation as a “holistic” food, i.e. one that provides a whole range of the nutrients that our body needs – in a balanced and tasty blend.

Health, Nutrition and Therapeutic Uses of Hemp Oil

The oils high in EFAs and GLA actually prevent, or even cure, a large number of illnesses has been shown in several clinical studies. The following lists a few of the successes.
Many “modern” health problems, including heart disease, obesity, skin diseases and certain cancers have been blamed on “too much of the wrong fats, not enough of the right ones” in our diet.
Health specialists now recommend that fat consumption be limited to no more than 30 percent of our total calorie intake. However, fats and oil are not only a source of energy, they also provide the necessary EFAs. Thus, if we eat fats, they should contain as much EFAs and other unsaturated fatty acids as possible…in the proper ratio. Their benefits have been proven in numerous clinical studies.
A variety of diseases can be successfully treated with GLA and linoleic acid, both well represented in hemp oil.


Patients with neurodermitis suffer from agonizing itching, especially at night. The skin feels very dry and the activity of perspiratory and sebaceous glands is low. Neurodermitis – as is psoriasis – is characterized by a high water loss through the skin. Deficiency in EFAs can be one of the main causes. Essential fatty acids have a strong influence on the barrier function of the skin, because they regulate water loss through the epidermis (outer layer of the skin).
Patients with neurodermitis show a deficiency of essential fatty acids which affects the whole body. It is assumed that low enzymatic activity leads to reduced transformation of linoleic acid to GLA and subsequently to prostaglandin deficiency. Hemp oil, due to its high content in both, linoleic and gamma-linolenic acid, thus can assist in the treatment of this disease. The daily oral dose found to improve skin condition over a twelve week period corresponds to 18 grams or about four teaspoons of hemp oil. Another study showed improved skin conditions through external application of an ointment containing gamma-linolenic acid.

Cardiovascular Diseases

Most of the cardiovascular diseases threatening the health of people around the world are caused by the formation of arterial plaque, i.e. the deposition of blood components on the interior walls of our blood vessels. This process may eventually block blood flow and cause arteriosclerosis and strokes.
LDL cholesterol, a sticky substance present in the blood, has been identified as one of the main contributors to arterial plaque formation. Among other factors, such as smoking and stress, the intake of the saturated fatty acids present in animal fat is known to contribute to a high LDL level in the blood. Reversely, dietary treatment of patients with daily doses of linoleic acid and GLA which correspond roughly to four teaspoons of hemp oil, has shown to rapidly decrease elevated blood levels of both, LDL cholesterol and total cholesterol. Thus, the replacement of oils and fats high in SaFA with hemp oil will help reduce the risk of arteriosclerosis and other cardiovascular diseases.


PMS, or premenstrual syndrome, can include varying intensities of painful muscular tension, swelling of the breast, tension and irritability as well as aggressiveness and depression.
Investigations indicate that women with PMS suffer from a fatty acid metabolism disorder, where the ability to convert linoleic acid into gamma-linolenic acid and subsequently into prostaglandins is impaired.
A daily dose of 1.37 grams linoleic acid and 156 milligrams GLA over a twelve-week period significantly improved the PMS related symptoms in clinical studies. This dose corresponds to one teaspoon of hemp oil a day.

Rheumatoid Arthritis

Some fatty acids, including gamma-linolenic acid, are indicated as effective anti-inflammatory and immune system stimulating factors. Daily oral administration of 1.2-1.4 grams of GLA (corresponding to eight teaspoons of hemp oil) over a period of twelve weeks significantly alleviated the symptoms of rheumatoid arthritis.

Other Diseases

Other studies suggest administration of EFAs and GLA as preventive measure and a treatment for multiple sclerosis, schizophrenic psychosis, and cancer.
Multiple sclerosis occurs more frequently in geographical regions where the diet includes high amounts of saturated fats. Dietary supplementation of unsaturated fatty acids may have a positive effect on the course of the disease.
In patients with schizophrenic psychosis disturbances are found in the fatty acid metabolism which might be treated through administration of essential fatty acids.
Cancer treatment may be assisted by administration of linoleic acid and GLA. Cancer tissue and cells have lower contents of GLA and other related metabolites compared to healthy tissue. Linoleic acid enhances die-off of cancer cells. Administration of this essential fatty acid might therefore prove to have positive effects.
Obviously, increasing the dietary intake of EFAs and GLA at the expense of SaFAs, is an effective way to prevent these and other diseases. Hemp oil used in the kitchen provides as much of the EFAs as necessary – in the right composition. Its delicious taste is the “icing on the cake”.
The following table shows the GLA and linoleic acid content in hemp oil in grams and teaspoons and allows you to determine desired dosages. As the GLA content in hemp oil may vary (refer to product label), so may the amount of oil required to achieve a certain dose.

Hemp Oil in Body Care Products

The increasing popularity of hemp oil in cosmetics is also largely due to its high EFA content. Facial creams, body lotions, soaps, lip balm, shampoo and conditioner, massage oil with hemp oil are just some of the available products.
As a natural ingredient in the formulation of cosmetics, hemp oil provides the following benefits:
  • The emollient, lubricant, and moisturizing properties of EFAs are well established. Although true EFA deficiency in humans is a rare condition, cosmetic skin problems such as scaling or dry, cracking skin also respond cosmetics containing EFAs. Because of their mobility, EFAs and GLA, counteract the ongoing loss of the skin’s natural barrier substance between the cells of the epidermis, thus preventing excessive moisture loss, dry-out, and cracking of the skin.
  • The slow-down with age in the metabolism of cells in the basal layer of the epidermis also reduces the amount of EFAs released into the epidermis. This age related decline in activity is a major contributor to the above mentioned detrimental effects to the skin, thus contributing to the formation of wrinkles and overall skin aging. Topical application of EFAs partially compensates for their decline in the skin and the obvious effects of aging.
Hemp oil provides an additional benefit over other seed oil containing EFAs and GLA. Even when grown conventionally, hemp farming does usually not involve the use of pesticides and herbicides.
Rather, it provides additional agricultural benefits, such as suppression of weeds and pests.
This compares favorably to evening primrose and borage, specialty cultures which are sensitive to pests and weeds and require, unless grown organically, the use of synthetic chemicals. Thus, the pesticide free production of hemp seeds renders their oil a “truly natural” alternative to other seed oils.

Oil Production and Quality

Many plant oils naturally contain unsaturated fatty acids. Unfortunately, a high content in polyunsaturated fatty acids, such as in hemp and flax oil, increases the tendency of an oil to become rancid, especially when exposed to oxygen, light, and elevated temperatures. Rancidity results from the breakdown of fatty acids causing formation of rancid tasting and unhealthy compounds, such as aldehydes.
Most edible oils on supermarket shelves have been treated by mechanical and chemical refining processes to increase their shelf-life, enhance clarity and remove other undesirable compounds. The latter may result from poor seed quality or from the extraction process. Commercial oil making may include any or all of the following steps: solvent extraction of oil from the ground seeds, de-gumming, alkali refining, bleaching deodorizing, hydrogenation, and others.
Margarines, shortenings, and shortening oils for example are hydrogenated – or hardened – which removes unsaturated fatty acids, including the essential fatty acids. During the refining processes aroma and flavour as well as valuable compounds, for example vitamin E, lecithin, and minerals are removed.
Trace amounts of solvents may be present, preservatives added, and some of these processes may even result in the formation of unhealthy by-products, for example trans-fatty acids from hydrogenation, or hardening, of oils. Manufacturers are not required to declare these processes on the label, so they don’t.
Until recently, almost all oils on supermarket shelves used to be solvent extracted and fully refined. Such commodity oils aren’t “poisonous”. In fact, they also reflect the trend towards oils with a higher content of unsaturated fatty acids, i.e. sunflower, canola. Yet, they are bland and are missing valuable ingredients and character.
No wonder cold pressed oils (olive, walnut, safflower, pumpkin) are increasingly gaining shelf space.
Mechanically cold-pressed (not solvent extracted), unrefined oils have the characteristic aroma and flavour of the seeds from which they were pressed. Hemp oil for example has a delicate, nutty flavour. Unrefined oils still contain most of the vitamins, other antioxidants and minerals present in the seeds.
These oils generally also have a high content of unsaturated fatty acids which increases their tendency to become rancid and thus reduces their shelf-life. To make the most of the natural and healthy ingredients of these oils, they should be consumed fresh.
Unrefined, cold-pressed oils – such as hemp oil – are routinely pressed and bottled in a nitrogen atmosphere and sold in tinted or dark bottles to protect them from light. After opening they should be stored in the refrigerator and consumed within six months.

The THC Issue

Health agencies and media routinely raise the question: do hemp seeds and oil contain too much tetrahydrocannabinol (THC), the psychoactive ingredient of marijuana? Even hemp oil from European or Chinese low-THC varieties of industrial hemp routinely contains traces of THC, though too low to cause any noticeable effects. Surveys typically find 5-20 ppm (mg/kg).
The Swiss government recently set a 50 ppm maximum limit for THC in food. This suggests that THC in hemp oil usually does not pose the risk of involuntary intoxication or other health risks. Health Canada has set a more conservative limit of 10 ppm which many imported oils may fail to meet.
However, there are several ways to further reduce the THC content of hemp oil and other foods from hemp seeds.
Hemp seeds themselves do not contain THC. Rather, it is present in the flowers and their sticky resins may leave traces of THC on the seeds.
It comes as no surprise that thorough cleaning of the seeds, or even de-hulling, and the use of varieties with a very low THC-content have proven effective in reducing THC levels in oil to less than 5 ppm. Hemp oil producers now increasingly turn to these methods.
To provide guidance to decision makers, the nova institute recently suggested THC limits for various food products. see e.g. at the website of the North American Industrial Hemp Council www.naihc.org They provide a wide margin of safety from psychoactive effects and can be met as long as seeds are properly cleaned and low-THC varieties are used.

Answers to Commonly Asked Questions

Is sale of hemp oil legal?
Yes. Hemp oil can be legally imported or pressed in Europe, and from imported, sterilized seeds in the USA and for external use only in Australia.

Does hemp oil make high?

No. The meat of hemp seed does not contain the drug tetrahydrocannabinol (THC), which is the psychoactive substance in marijuana. Minute amounts of THC may be transferred from the flowers surrounding the leaves into the oil during pressing.
However, these trace amounts are, if seeds from low-THC varieties are used and properly cleaned, too low to have any psychoactive effects.

Can hemp oil be used for frying or deep-frying?

Better not. Unrefined hemp oil – just like olive oil – should not be used for high temperature or deep-frying. At high temperatures, unhealthy oxidation and polymerization products are formed from the unsaturated fatty acids. Furthermore, at temperatures approaching 400 F, undesirable trans-fatty acids are gradually formed. Quick sautéing is acceptable, yet care must be taken to keep the oil from smoking.Flax oil also has a high content in unsaturated essential fatty acids.

What is the benefit of hemp oil?

The ratio of the essential fatty acids (three parts linoleic acid to one part alpha-linolenic acid) in hemp oil is favourable for the human body because it matches its nutritional requirements. Flax oil, despite its higher essential fatty acid content, has a less favourable ratio (1:5). Flax oil also does not contain gamma-linolenic acid, an unsaturated fatty acid, which is found abundantly in hemp oil.

To maintain maximum freshness refrigerate after opening and use within six months.

Further Reading
Paul Benhaim: Modern Introduction to Hemp 2004
Paul Benhaim: Healthy Eating Made Possible. Vision Paperbacks 2000
Udo Erasmus: Fats that heal, fats that kill. Alive Books, 1994.
Jean-Luc Deferne, David W. Pate: Hemp seed oil: A source of valuable essential fatty acids. Journal of the International Hemp Association, Volume 3, Number 1, Pages 1-7, 1996.
Helga Mˆlleken, Roland R. Theimer: Survey of minor fatty acids in Cannabis sativa L. fruits of various origins. Journal of the International Hemp Association, Volume 4, Number 1, Pages 13-17, 1997.
Yung-Sheng Huang, David E. Mills: g-linolenic acid: Metabolism and its role in nutrition and medicine.
AOCS Press, 1996.
EFA: essential fatty acid
UFA: unsaturated fatty acid
PuFA: polyunsaturated fatty acid
SaFA: saturated fatty acid
THC: tetrahydrocannabinol

Thursday, January 16, 2014

Adopt a Colorado Industrial Hemp Seed/Plant/Farmer 2014

This is an Excellent Opportunity for People to Take Part of the Industrial Hemp Movement in Colorado, Without having to Move to Colorado!  

Hemp Seed is the Super Food Seed with a multitude of various uses. Hemp, before prohibition was use for many common products such as rope, fabric, paper, canvas, etc. Due to prohibition, only non viable hemp seeds could be exported from places like Canada, Chine, Europe etc. Thanks to the legalization of hemp in Colorado and other states, soon decriminalization on a federal level, the industry can again emerge.
Adopt a Colorado Industrial Hemp Seed/Plant/Farmer or a make a bigger donation and support Colorado's hemp farmers 2014, hemp events by GrowHempColorado.com and further seed development.
Options are below. Have a happy hemp day.

Please be Sure to Share with your Friends!

Adopt a Hemp Plant/Seed

Adopt/Sponsor a Colorado Industrial Hemp Plant/Seed ($10)
Now your can show your hemp pride from any state!
You will receive a pic and monthly updates on your seed/plant
Checks can be sent to: PO Box 128 Erie, CO 80516
Read More HERE about the Hemp Seed/Plant.

Adopt 10 Hemp Seeds/Plants

Adopt/Sponsor a Colorado Industrial Hemp Plant/Seed
(10 Seed/plants = $100) Now your can show your hemp pride from any state!
You will receive a pic and monthly updates on your seed/plant

Checks can be sent to: PO Box 128 Erie, CO 80516 Read More HERE about the Hemp Seed/Plant.

Sponser a Hemp Farmer/Efforts/Seed Production

Sponsor a Colorado Hemp Farmer/Efforts/Seed Production
(any amount you decide) Now your can show your hemp pride from any state!
Amounts over $1000 will also receive info on your sponsored hemp farmer and/or activities. + 1 lb bag of Colorado Hemp Coffee and and other surprise hemp gifts.

Checks can be sent to: PO Box 128 Erie, CO 80516 Read More HERE about the Hemp Seed/Plant.


Hemp Healthy Cooking: Hemp for Breakfast

  • Cooking Time: 2-5 Min.
  • Servings: 1
  • Preparation Time:2-5 Min.

Hemp Healthy Cooking: Hemp for Breakfast


  • Oatmeal
  • Honey
  • Hulled Hemp seed


  • Just add 1/8 cup hulled hemp seed to your morning oatmeal
  • add 2-3 tablespoons of honey
  • add a splash of hemp milk optional
  • add some berries of choice, I like Blue berries in mine.
  • Sprinkle additional hemp seed on top.

Hemp Healthy Cooking: Hemp for Breakfast


Simply the Best and easiest way to get your hemp and honey fix.
Author Credit: Derek Cross
What's New on BakeSpace TV

- See more at: http://www.bakespace.com/recipes/detail/Savory-Oatmeal-with-Hulled-Hemp-Seed-%26-Honey/53461/#sthash.TBqJCI0O.dpuf


Cooking Time: 10-15 Min. Servings: 4 servings Preparation Time: 10 Min.


  • 1 pound white button mushroom
  • 1 shallot or small sweet onion sliced small
  • 1/8 cup of olive oil
  • 2-3 teaspoons chopped basil
  • About 1/8 cup rice wine vinegar
  • 1-2 tablespoons hulled hemp seed
  • 2-3 tablespoons hemp oil


  • Clean and wash mushrooms
  • Slice shallots or sweet onion
  • Heat skillet over high heat add olive oil (never fry with hemp oil)
  • Add mushrooms top hot pan to darken mushrooms
  • Add onions
  • Add chopped fresh basil
  • Let cook while stirring
  • After mushrooms are colored and onions are cooked down
  • Add about 1/8 cup rice wine vinegar around outside edge of pan
  • Let vinegar evaporate while stirring
  • Add few more swirls of olive oil
  • Remove off heat and add 1/8 cup hemp oil
  • Add 1/3 cup hemp seed
  • And stur
  • Eat warm and serve over your favorite pasta, or eat by itself as quick mushroom meal
  • Best if you let mushrooms marinate a day or two and serve later
  • The hemp seed and oil give this mushroom a nice nutty smokey flavor!
  • Enjoy


I love marinated mushrooms over a thick stringy pasta!
Author Credit: Derek Cross
What's New on BakeSpace TV

Wednesday, January 15, 2014

Brain Trauma--Medical Marijuana

By Debbie Wilson on September 8, 2012  From noahsarkconsulting.blogspot.com
Brain Trauma--Medical Marijuana

Published by Jan

BRAIN TRAUMA-How Does Medical Marijuana Help?
Traumatic brain injury (TBI), also known as intracranial injury, occurs when an external force traumatically injures the brain.  TBI can be classified based on severity, mechanism (closed or penetrating head injury), or other features (e.g. occurring in a specific location or over a widespread area).  Head injury usually refers to TBI, but is a broader category because it can involve damage to structures other than the brain, such as the scalp and skull.
BI is a major cause of death and disability worldwide, especially in children and young adults.  Causes include falls, vehicle accidents, and violence.  Prevention measures include use of technology to protect those who are in accidents, such as seat belts and sports or motorcycle helmets, as well as efforts to reduce the number of accidents, such as safety education programs and enforcement of traffic laws.
Brain trauma can be caused by a direct impact or by acceleration alone.  In addition to the damage caused (at the moment) of injury, brain trauma causes secondary injury, a variety of events that take place in the minutes and days following the injury.  These processes, which include alterations in cerebral blood flow and the pressure within the skull, contribute substantially to the damage from the initial injury.
TBI can cause a host of physical, cognitive, emotional, and behavioral effects, and outcome can range from complete recovery to permanent disability or death.  The 20th century saw critical developments in diagnosis and treatment  which decreased death rates and improved outcome.  These include imaging techniques such as computed tomography and magnetic resonance imaging.  Depending on the injury, treatment required may be minimal or may include interventions such as medications and emergency surgery.  Physical therapy,  speech therapy,  recreation therapy,  and occupational therapy  for rehabilitation.
Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile.  Brain function is temporarily or permanently impaired and structural damage may or may not be detectable with current technology.
BI is one of two subsets of acquired brain injury (brain damage that occurs after birth);  the other subset is non-traumatic brain injury, which does not involve external mechanical force (examples include stroke and infection).   All traumatic brain injuries are head injuries, but the latter term may also refer to injury to other parts of the head.   However, the terms head injury and brain injury are often used interchangeably.   Similarly, brain injuries fall under the classification of central nervous system injuries  and neurotrauma.   In neuropsychology research literature, the term "traumatic brain injury" generally is used to refer to non-penetrating traumatic brain injuries.
TBI is usually classified based on severity, anatomical features of the injury, and the mechanism (the causative forces).   Mechanism-related classification divides TBI into closed and penetrating head injury.   A closed (also called nonpenetrating, or blunt) injury occurs when the brain is not exposed.   A penetrating, or open, head injury occurs  when an object pierces the skull and breaches the dura mater, the outermost membrane surrounding the brain.
Brain injuries can be classified into mild, moderate, and severe categories.   The Glasgow Coma Scale (GCS), the most commonly used system for classifying TBI severity, grades a person's level of consciousness on a scale of ( 3–15) based on verbal, motor, and eye-opening reactions to stimuli.   It is generally agreed that a TBI with a GCS of 13 or above is mild, 9–12 is moderate, and 8 or below is severe.   Similar systems exist for young children.   However, the GCS grading system has limited ability to predict outcomes.  Because of this, other classification systems such as the one shown in the table are also used to help determine severity.  A current model developed by the Department of Defense and Department of Veterans Affairs uses all three criteria of GCS after resuscitation, duration of post-traumatic amnesia (PTA), and loss of consciousness (LOC).   It also has been proposed to use changes which are visible on neuroimaging, such as swelling, focal  lesions, or diffuse injury as method of classification.   Grading scales also exist to classify the severity of mild TBI, commonly called concussion;  these use duration of LOC, PTA, and other concussion symptoms
Systems also exist to classify TBI by its pathological features.   Lesions can be extra-axial, (occurring within the skull but outside of the brain) or intra-axial (occurring within the brain tissue).   Damage from TBI can be focal or diffuse, confined to specific areas or distributed in a more general manner, respectively.   However it is common for both types of injury to exist in a given case
Signs and symptoms                     

Unequal pupil size is a sign of a serious brain injury.  Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected.  Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right.   Symptoms are also dependent on the injury's severity.  With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes.   Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing,  lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.   Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking.   Mild TBI symptoms may also be present in moderate and severe injuries
A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken, dilation of one or both pupils, slurred speech, aphasia (word-finding difficulties), dysarthria (muscle weakness that causes disordered speech), weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation.  Common long-term symptoms of moderate to severe TBI are changes in appropriate social behavior, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning.   Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in (60.9%)  of individuals with TBI.  Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved with appropriate rehabilitation.  One of two subsets of acquired brain injury (brain damage that occurs after birth);  the other subset is non-traumatic brain injury, which does not involve external mechanical force (examples include stroke and infection).   All traumatic brain injuries are head injuries, but the latter term may also refer to injury to other parts of the head.   However, the terms head injury and brain injury are often used interchangeably.   Similarly, brain injuries fall under the classification of central nervous system injuries  and neurotrauma.   In neuropsychology research literature, the term "traumatic brain injury" generally is used to refer to non-penetrating traumatic brain injuries.
When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly.  Signs of increased ICP include decreasing level of consciousness, paralysis or weakness on one side of the body, and a blown pupil, one that fails to constrict in response to light or is slow to do so.  Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP.  Anisocoria, unequal pupil size, is another sign of serious TBI.  Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.
Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them.  Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat, and irritability.
The most common causes of TBI include violence, transportation accidents, construction, and sports.  In the US, falls account for( 28%) of TBI,  motor vehicle (MV) accidents for (20%),  being struck by an object for (19%),  violence for ( 11%),  and non-MV bicycle accidents for ( 3%).  Bicycles and motor bikes are major causes, with the latter increasing in frequency in developing countries.  The estimates that between  (1.6 and 3.8)  million traumatic brain injuries each year are a result of sports and recreation activities in the US.  In children aged two to four, falls are the most common cause of TBI, while in older children bicycle and auto accidents compete with falls for this position.  TBI is the third most common injury to result from child abuse.  Abuse causes  (19%)  of cases of pediatric brain trauma, and the death rate is higher among these cases.  Domestic violence is another cause of TBI, as are work-related and industrial accidents.  Firearms and blast injuries from explosions are other causes of TBI,  which is the leading cause of death and disability in war zones.   According to Representative Bill Pascrell (Democrat, NJ), TBI is "the signature injury of the wars in Iraq and Afghanistan."
Physical forces
Ricochet of the brain within the skull may account for the “coup-contrecoup phenomenon”.
The type, direction, intensity, and duration of forces all contribute to the characteristics and severity of TBI. Even in the absence of an impact, significant acceleration or deceleration of the head can cause TBI, however in most cases a combination of impact and acceleration is probably to blame.
The violent shaking of an infant that causes shaken baby syndrome commonly manifests as diffuse injury. In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage.  Shock waves caused by penetrating injuries can also destroy tissue along the path of a projectile, compounding the damage caused by (the missile)  itself.
Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup)  injury).  When a moving object impacts the stationary head, coup injuries are typical Contrecoup injuries are usually produced when the moving head strikes a stationary object.
Forces involving the head striking or being struck by something, termed contact or impact loading, are the cause of most focal injuries, and movement of the brain within the skull, termed noncontact or inertial loading, usually causes diffuse injuries.
Secondary injury events include damage to the blood–brain barrier, release of factors that cause inflammation, free radical overload, excessive release of  the neurotransmitter glutamate (excitotoxicity),  influx of calcium and sodium ions into neurons, and dysfunction of mitochondria.  Injured axons in the brain's white matter may separate from their cell bodies as a result of secondary injury, often  killing those neurons.  Other factors in secondary injury are changes in the blood flow to the brain;ischemia (insufficient blood flow);  cerebral hypoxia (insufficient oxygen in the brain);  cerebral edema (swelling of the brain);  and raised intracranial pressure (the pressure within the skull).   Intracranial pressure may rise due to swelling or a mass effect from a lesion, such as a hemorrhage.
Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected outcome in the long term.  It is more useful than CT for detecting injury characteristics .
Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments to give. Neuropsychological assessment are  performed to evaluate the long-term cognitive sequels and to aid in the planning of the rehabilitation
Omega-3 DHA offers protection against the biochemical brain damage that occurs after a traumatic injury. Rats given DHA prior to induced brain injuries suffered smaller increases in two key markers for brain damage (APP and caspase-3), as compared with rats given no DHA.
It is important to begin emergency treatment within the so-called "golden hour" following the injury.
In the  acute stage,  the primary aim of the medical personnel is to stabilize the patient and focus on preventing further injury because little can be done to reverse the initial damage caused by trauma.  Rehabilitation is the main treatment for the subacute and chronic stages of recovery.  International clinical guidelines have been proposed with the aim of guiding decisions in TBI treatment, as defined by an authoritative examination of current evidence.
Acute stage                                                                            
Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center.  Both during transport and in hospital the primary concerns are ensuring proper oxygen supply, maintaining adequate cerebral blood flow, and controlling raised intracranial pressure (ICP),  since high ICP deprives the brain of badly needed blood flow and can cause deadly brain herniation. Other methods to prevent damage include management of other injuries and prevention of seizures.
Chronic stage
Physical therapy will commonly include muscle strength exercise.
Once medically stable, patients might be transferred to a subacute rehabilitation unit of the medical center or to an independent rehabilitation hospital.  Rehabilitation aims to improve independent function at home and in society and to help adapt to disabilities.   A multidisciplinary approach is key to optimising outcome.
Pharmacological treatment can help to manage psychiatric or behavioral problems.  Medication is also used to control post-traumatic epilepsy;  however the preventive use of anti-epileptics is not recommended.  In those cases where the person is bedridden due to a reduction of consciousness, has to remain in a wheelchair because of mobility problems, or has any other problem heavily impacting self-caring capacities, care giving and nursing are critical.  Improvement of neurological function usually occurs for two or more years after the trauma.  For many years it was believed that recovery was  fastest during the first six months, but there is no evidence to support this.  It may be related to services commonly being withdrawn after this period, rather than any physiological limitation to further progress.  Children recover better in the immediate time-frame and improve for longer periods.  Complications are distinct medical problems that may arise because of the TBI.  The results of traumatic brain injury vary widely in type and duration;  they include physical, cognitive, emotional, and behavioral complications.  TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a state of alertness to interact with their surroundings),  and minimally conscious state (in which patients show minimal signs of being aware of self or environment).  Lying still for long periods can cause complications including pressure sores, pneumonia or other infections, progressive multiple organ failure,  and deep venous thrombosis, which can cause pulmonary embolism.  Infections that can follow skull fractures and penetrating injuries include meningitis and abscesses.   Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke.. Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), myoclonus (shock-like contractions of muscles), and loss of movement range and control (particularly with a loss of movement repertoire).  The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas.  People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma).  People may lose or experience altered vision, hearing, or smell.
Hormonal disturbances may occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients.  Development of diabetes insipidus or an electrolyte  abnormality acutely after injury indicate need for endocrinologic work up.  Signs and symptoms of hypopituitarism may develop and be screened for in adults with moderate TBI and in mild TBI with imaging abnormalities.  Children with moderate to severe head injury may also develop hypopituitarism.  Screening should take place 3 to 6 months, and 12 months after injury.
Cognitive deficits that can follow TBI include impaired attention;  disrupted insight, judgement, and thought;  reduced processing speed;  distractibility;  and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking.  Memory loss, the most common cognitive impairment among head-injured people, occurs in (20–79%)  of people with closed head trauma, depending on severity.  People who have suffered TBI may also have difficulty with understanding or producing spoken or written language, or with more subtle aspects of communication such as body language.  Post-concussion syndrome, a set of lasting symptoms experienced after mild TBI  may include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression.  Multiple TBIs may have a cumulative effect.  A young person who receives a second concussion before symptoms from another one have healed may be at risk for developing a very rare but deadly condition called second-impact syndrome,  where the brain swells catastrophically after even a mild blow, with debilitating or deadly results.  About one in five career boxers is affected by chronic traumatic brain injury (CTBI), which causes cognitive, behavioral, and physical impairments.   Dementia pugilistica, the severe form of CTBI, primarily affects career boxers,  years later.  It commonly manifests as dementia, memory problems, and parkinsonism (tremors and lack of coordination) .  BI may cause emotional or behavioral problems and changes in personality.  These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, and anger.  TBI appears to predispose a person to psychiatric disorders  including obsessive compulsive disorder, alcohol or substance abuse or dependence, dysthymia, clinical depression, bipolar disorder, phobias, panic disorder, and schizophrenia.  Behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, and changes in personality.  Different behavioral problems are characteristic of the location of injury;  for instance, frontal  lobe injuries often result in disinhibition and inappropriate or childish behavior, and temporal  lobe injuries often cause irritability and aggression.  In patients who have depression after TBI, suicidal ideation is not uncommon; the suicide rate among these persons is increased two to three fold.
TBI also has a substantial impact on the functioning of family systems.   Caregiving family members and TBI survivors often significantly alter their familial roles and responsibilities following injury, creating significant change and strain on a family system.  Typical challenges identified by families recovering from TBI include:  frustration and impatience with one another, loss of former lives and relationships, difficulty setting reasonable goals, inability to effectively solve problems as a family, increased level of stress and household tension, changes in emotional dynamics, and overwhelming desire to return to pre-injury status. Additionally, families may exhibit less effective functioning in areas including coping, problem solving and communication.  Psychoeducation and counseling models have been demonstrated to be effective in minimizing family disruption.
TBI is a leading cause of death and disability around the globe and presents a major worldwide social, economic, and health problem.   It is the number one cause of coma,  it plays the leading role in disability due to trauma  and is the leading cause of brain damage in children and young adults . In Europe  it is responsible for more years of disability than any other cause.  It also plays a significant role in half of trauma deaths.  A World Health Organization study estimated that between 70 and 90%  of head injuries that receive treatment are mild,  and a US study found that moderate and severe injuries each account for 10% of TBIs, with the rest mild.                           
In the US, the mortality (death) rate is estimated to be 21% by 30 days after TBI.   A study on Iraq War soldiers found that severe TBI carries a mortality of 30–50%.   Deaths have declined due to improved treatments and systems for managing trauma in societies wealthy enough to provide modern emergency and neurosurgical services.  The fraction of those who die after being hospitalized with TBI fell from almost half in the 1970s to about a quarter at the beginning of the 21st century.  This decline in mortality has led to a concomitant increase in the number of people living with disabilities that result from TBI.
Biological, clinical, and demographic factors contribute to the likelihood that an injury will be fatal.  In addition, outcome depends heavily on the cause of head injury.  In the US, patients with fall-related TBIs have an  89%  survival rate, while only 9% of patients with firearm-related TBIs survive.  In the US, firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls.  Of deaths from firearms, 75%  are from suicides.  The incidence of TBI is increasing globally, largely due to an increase in motor vehicle use in low and middle  income countries .
TBI is present in  (85%) of traumatically injured children, either alone or with other injuries.  The greatest number of TBIs occur in people aged ( 15–24).  Because TBI is more common in young people, its costs  to society are high,  due to the loss of productive years,  to death and disability.  The age groups most at risk for TBI are children ages (5-9) and adults over age ( 80),  and the highest rates of death and hospitalization due to TBI are in people over age ( 65).  The incidence of fall-related TBI in First World countries is increasing as the population ages;  thus,  the median age of people with head injuries has increased.
Regardless of age, TBI rates are higher in males.  I n the 1970s , awareness of TBI as a public health problem grew,  and a great deal of progress has been made since then in brain trauma research,  such as the discovery of primary and secondary brain injury.  The 1990s  saw the development and dissemination of standardized guidelines for treatment of TBI, with protocols for a range of issues such as drugs  and management of intracranial pressure.  Research since the early 1990s  has improved TBI survival;  that decade was known as the "Decade of the Brain" for advances made in brain research.  No medication exists to halt the progression of secondary injury, but the variety of pathological events presents opportunities to find treatments that interfere with the “damage processes” .
Hyperbaric oxygen therapy (HBO) for TBI has remained controversial as studies have looked for improvement mechanisms, for the delivery of the oxygen, and further evidence shows that it may have potential as a treatment.
How can Medical Marijuana help TBI patients?
Natural endogenous cannabinoids are produced in the bodies of humans and some animals. Their main function is to bind to cannabinoid receptors in the body of the organism they came from.
A compound the brain manufactures in response to trauma may be useful as a treatment for complications resulting from brain injury, Israeli researchers report.
“``We believe that this compound, that the brain itself produces, may serve as a neuroprotectant agent,'' lead author Esther Shohami, a professor in the School of Pharmacy at the Hebrew University in Jerusalem, told Reuters Health.
The compound, known as 2-arachidonoyl glycerol (2-AG), is a cannabinoid, a substance the body produces with a similar structure to chemicals found in the cannabis plant, the source of marijuana.
In research published in the October 4th issue of Nature, the investigators found 2-AG at 10 times the normal level in the brains of mice 4 hours after a traumatic injury.
The researchers theorize that the compound somehow helps prevent some of the secondary complications associated with brain injury, possibly by reducing the inflammatory response, slowing the production of a toxic brain chemical or boosting the blood supply to the brain immediately after the injury.
However, the natural amounts the brain cells produce following trauma probably do not reach high enough levels to be effective, Shohami noted.
To investigate the effects of the compound, the researchers synthesized 2-AG and injected it an hour after brain injury had been induced in mice. The mice were evaluated 1, 4 and 7 days after injury.
``We found a tremendous improvement in the recovery of the mice,'' Shohami said, noting that there was less excess fluid causing swelling in the brain, better recovery of motor function, and fewer dead brain cells and brain tissue.
However, the drug's protection against neurological damage was short-lived, with significant effects lasting only a day after treatment.
Shohami said she hopes to eventually investigate the compound on humans who have suffered brain injuries and to extend the timeframe in which the substance could be offered.
``Its administration, as a single injection, should be considered as a novel therapeutic modality,'' she said. ``Since the benefit was achieved by a single administration, I do not expect serious side-effects or toxicity to be a major problem.''
Cannabis & Neuroprotection
Not only has modern science refuted the notion that marijuana is neurotoxic, recent scientific discoveries have indicated that cannabinoids are, in fact, neuroprotective, particularly against alcohol-induced brain damage.  In a recent preclinical study -- the irony of which is obvious to anyone who reads it -- researchers at the US National Institutes of Mental Health (NIMH) reported that the administration of the non-psychoactive cannabinoid cannabidiol (CBD) reduced ethanol-induced cell death in the brain by up to 60 percent. "This study provides the first demonstration of CBD as an in vivoneuroprotectant ... in preventing binge ethanol-induced brain injury," the study's authors wrote in the May 2005 issue of the Journal of Pharmacology and Experimental Therapeutics.  Alcohol poisoning is linked to hundreds of preventable deaths each year in the United States, according to the Centers for Disease Control, while cannabis cannot cause death by overdose.
(Of course), many US neurologists have known about cannabis' neuroprotective  ‘”powers”  for years.  NIMH scientists in 1998 first touted the ability of natural cannabinoids to stave off  the brain-damaging effects of stroke and acute head trauma.  Similar findings were then replicated by investigators in the Netherlands,  then Italy and, most recently, by Japanese research in 2005.  However, attempts to measure the potential neuroprotective effects of synthetic cannabinoid-derived medications in humans have so far been inconclusive.
Cannabis & Cognition
What about claims of cannabis' damaging effect of cognition?  A review of the scientific literature indicates that rumors regarding the "stoner stupid" stereotype are unfounded.  According to clinical trial data published this past spring in the American Journal of Addictions, cannabis use -- including heavy, long-term use of the drug -- has, at most, only a negligible impact on cognition and memory.  Researchers at Harvard Medical School performed magnetic resonance imaging on the brains of ( 22) long-term cannabis users (reporting a mean of  (20-100)  lifetime episodes of smoking)  and (26) controls (subjects with no history of cannabis use).  Imaging displayed "no significant differences" between heavy cannabis smokers compared to controls.
Previous trials tell a similar tale.  An October 2004 study published in the journal Psychological Medicine examining the potential long-term residual effects of cannabis on cognition in monozygotic male twins reported "an absence of marked long-term residual effects of marijuana use on cognitive abilities."  A 2003 meta-analysis published in theJournal of the International Neuropsychological Society also "failed to reveal a substantial, systematic effect of long-term, regular cannabis consumption on the neurocognitive functioning of users who were not acutely intoxicated," and a 2002 clinical trial published in the Canadian Medical Association Journal determined,  "Marijuana does not have a long-term negative impact on global intelligence."
Finally, a 2001 study published in the journal Archives of General Psychiatry found that long-term cannabis smokers who abstained from the drug for one week  "showed virtually no significant differences from control subjects (those who had smoked marijuana less than 50 times in their lives) on a battery of 10 neuropsychological tests.”   Investigators further added, "Former heavy users, who had consumed little or no cannabis in the three months before testing, [also] showed no significant differences from control subjects on any of these tests on any of the testing days."
As baby boomers age, the percentage of clients who may have used marijuana has increased (or one could simply have a practice in California).  In defense of TBI claims, defense attorneys will latch upon any allegations or proof  that the client has or does smoke marijuana. This can come up through direct testimony of the Plaintiff, testimony from friends or relatives, a failed drug test or from medical records.
In most jurisdictions the admissibility of this information would be subject to the balancing test of whether the probative value of such information outweighs the prejudicial effect of such information on the jury. The defense will try to establish that the use of marijuana is relevant because of the following:
• (it) had a downward effect on neuropsychological tests battery results;
• (it) adversely affects the recovery of the client from TBI;.
• (it) adversely affects wage and job aspects of the claim.
However,  recent medical research can be cited by the Plaintiffs to suggest that the active ingredient in marijuana “cannabinoids” are now thought to play an important role in actually protecting the brain from neuro-trauma  following injury.  The research cited below should be used to offset the mild amount of research that can be thrown towards the Plaintiff to suggest decreased recovery or test results due to occasional marijuana use.  If other (Plaintiff or defense) physicians have the research cited below, they can address the possible protective effects of the marijuana use and thus neutralize or take away the defenses ability to have the whole issue become admissible at trial.  The research is as follows:
• “Endocannabinoids and Traumatic Brain Injury” (Mechoulam, R 2007). This study showed that there are various neuro-protective effects of cannabinoids.
• “The Therapeutic Potential of the Cannabinoids in Neuroprotection” (Grundy RI, 2002).  The study cites the ability of cannabinoids to modulate neurotransmission and to act as anti-inflammatory and antioxidative agents.  Both post :  trauma inflamation and post traumatic oxidation are methods of secondary brain injury following the acute phase.
• “Therapeutic Potential of Cannabinoids in CNS Disease” (Croxford JL, 2003).  This study found that evidence suggest cannabinoids may prove useful in Parkinson’s disease in that dexanadinol (HU-211), a synthetic cannabinoid, is currently being assessed in clinical trial for traumatic brain injury and stroke.
• “Cannabinoids as Therapeutic Agents for Ablating Neuroinflammatory Disease” (Cabral GA et al. 2008).  Studying the early phases of post traumatic brain inflammation they noted that the cannabinoids receptor system may prove therapeutically manageable in reducing neuropathogenic disorders including closed head injuries.
Using some of the above research,  a ( Motions in Limine)  should be drafted to exclude any reference to marijuana use, arguing that any “adverse” consequence of use, is countered by its possible “benefit” and that the whole issue is based upon criminalizing the plaintiff.
Research has begun to accumulate over the past few years showing that cannabinoids are neuroprotective against brain injury resulting from toxins, hypoxia, and head trauma.  Cannabinoids are, loosely, chemicals that are similar in structure to the psychoactive components in cannabis and/or chemicals that activate the cannabinoid receptor system in the body.  Researchers have found protective effects not only from the plant-derived cannabinoids such as THC, but also from endogenous cannabinoids (those occurring naturally in the body, such as anandamide) and some synthetic pharmaceutical cannabinoids.
The research with the cannabis-source cannabinoids,    conducted in mice, rats, and in vitro, has shown remarkable effectiveness in reducing brain damage from injected toxins, hypoxia, and head trauma.  Other research has found that anandamide levels in the brains of rats naturally rise after brain injury or death and the cannabinoid system may play a primary role in limiting brain damage.
Because psychoactivity is considered an unwanted side effect, much of the current research is being done with synthetic cannabinoid system agonists.  One synthetic cannabinoid, Dexanabinol (HU-211),  is already in (phase 3)  trials (medium scale, involving humans) headed towards governmental approval as a neuroprotective pharmaceutical.  Research conducted in Israel that gave 67 patients with serious head trauma either Dexanabinol or placebo confirms similar research in rats showing reduced damage and faster recovery among those receiving the cannabinoids.  Although other promising head trauma treatments have failed in the demanding and complex  (phase 3)  research trials, many interested in the field of neuroinjury are excited about the findings to date.
The mechanisms by which the cannabinoids reduce damage from both toxic and traumatic injury to the brain are not fully understood.   Although some researchers have suggested that the cannabinoids may offer protection through a strong antioxidant effect, this is now considered unlikely to account for much of the protection, since cannabinoid-receptor antagonists block the beneficial effects and the doses of the cannabinoids given are very low.
Perhaps the current best guess for how these chemicals provide their protective effects is that their general dampening of neural activity reduces excitotoxicity (damage caused by overly excited neurons).  One of the
specific ways this happens is through the inhibition of the glutamate system in the brain.  The glutamatergic neurons are part of the excitatory system in the brain;  inhibiting glutamate reduces the activity of other neurons.   At least in some parts of the brain, activation of the CB1 cannabinoid receptor (a specific type of cannabinoid receptor) was shown to block pre-synaptic release of glutamate.  CB1 receptor activation is known to inhibit certain calcium channels, directly reducing the production of nitric oxide and other potentially damaging reactive oxygen agents.

Colorado Leading the Nation in Industrial Hemp Seed 2014 : Grow Hemp Colorado is the Nations 1st. Industrial Hemp Seed Provider

Origin: Colorado, Doesn't get much more Historical than That! This is an Amazing Event in America, just getting ready to map the process for American Hemp! Priceless!


  With all of the Nation focusing on Colorado's, "New Recreation Marijuana Laws", American's ALSO Need to be informed about Industrial Hemp in Colorado.  This means BIG Industry for Colorado!!!  With over 50,000 Uses of Industrial Hemp, It takes an Extremely Large Amount of Hemp Seed to get Started.
  Grow Hemp Colorado, has become the First in Industrial Hemp Seed Providers within the State of Colorado and not to mention the United States, lead by, Veronica Carpio.  She is a Pioneer in the Colorado Industrial Hemp Movement.

Photo: CONGRATULATIONS, Veronica Carpio, on Becoming the First licensed Hemp Seed Provider in Colorado!!  WooHoo
(CONGRATULATIONS, Veronica Carpio, on Becoming the First licensed Hemp Seed Provider in Colorado!!)

Hemp Seed & Plants

Hemp Seed is the Super Food Seed with a multitude of various uses. Hemp, before prohibition was use for many common products such as rope, fabric, paper, canvas, etc. Due to prohibition, only non viable hemp seeds could be exported from places like Canada, Chine, Europe etc. Thanks to the legalization of hemp in Colorado and other states, soon decriminalization on a federal level, the industry can again emerge.
Seed is the key....available seed is a rare commodity in America but it is the essential building block to the foundation of a new industry. Unfortunately due to existing international, federal and interstate issues, the State of Colorado hands are tied in helping import hemp seed. Fortunately, there are a handful of individuals in Colorado that have various strains of viable hemp seeds.
GrowHempColorado.com is a resource which can help any individual, farmer, business, or other interested party get connected with Colorado hemp seeds and plants. Suppliers & or resellers of Colorado hemp seed must be registered with the Colorado Department of Agriculture.
HOW YOU CAN PARTICIPATE NOW - Because seed is critical for the 2014 Colorado Hemp growing season, we are looking for interested parties who have locations which indoor efforts can be done to ensure additional seed by March 2014. These efforts must start immediately, in addition to mother plants being grown and cuttings from those plants also need to began getting ready for those who intend on applying for a Hemp Farming or Research & Development License from the Colorado Department of Agriculture.
It is more then possible for Colorado citizens to work together and ensure that we have a good year of planting, harvesting, testing, research, development and overall beginning view of that what the end result of a season looks like on a larger scale. The goal is at least 200K+ plants cuttings to be rooted and ready for planting by March.
Grow Hemp Colorado is offering seed at 50% off for any of those who would like to collaborate in cultivating seed at your location as well as grow mother plants which can be cloned.  In return Grow Hemp Colorado is asking for 50-50 share on both the seed harvest and rooted clones. Please contact Veronica at info@growhempcolorado.com This email address is being protected from spambots. You need JavaScript enabled to view it. or at 20.401.5609 to start participating today.
We are also looking for land which can be leased for a reasonable price and or donated for the first year, so interested parties who get licensed for farming and R&D in March 2014 can have a co-op location to share. Please contact us directly to discuss further if you are a interested land owner or investor. Grow Hemp Colorado is making all efforts to secure an number of these shared locations through out Colorado and as we make head way, we will post updates on this page and send email notifications, please be sure that are subscribed to our newsletter/email updates.
Please note: The Colorado Dept of Ag. is well aware of our ongoing efforts to accumulate/cultivate seed for the 2014 season and so far is in support of these efforts so far. They are the best government body we have ever worked with!