 |
| Magical mystical hemp forest. |
This time I'm trying to cure it (or at least minimize it) at home with all natural stuff. So far I've tried lavender, rosemary, and clary sage essential oils, homemade calendula-infused sweet almond oil, and the ponderosa pine-infused oil I made awhile back that's supposed to be awesome for skin conditions. The only thing I accomplished with those is to further irritate my skin. Finally, I went back to the tried and true: HEMP SEED OIL. I swear to god, this oil is magic. It cures EVERYTHING!
The information I give below applies to any type of skin inflammation, not just hives. Hemp works GREAT for dry, itchy skin, eczema... etc.
 |
| Mine's not this bad, but this is what cold urticaria looks like. Nice, right? |
How?
Just rub a half teaspoon or so on there after a shower in the morning and before bed at night. Also, take a teaspoon of it a day internally. I put it on my salads.WHY? I want to know.
First, What is urticaria? What exactly happens when you get hives?
Basically, urticaria is an inflammation process that is set in motion by whatever allergen/stimulus your body decides on. It is unknown why cold causes urticaria in some patients (Yay!!!). The process can be summed up like this:
- Mast cells in the skin are activated. They degranulate, and secrete histamine, leukotrienes, platelet activating factor (PAF), enzymes such as tryptase and chymase, cytokines, and chemotactic cytokines (chemokines);
- This causes capillary dilation. Arterioles, small branches of arteries that lead to capillaries that supply blood to the damaged region dilate, resulting in increased blood flow. Lymph capillaries also dilate, causing increased lymphatic fluid to enter the area;
- The capillaries become more permeable, so lymph fluid (white blood cells) and blood proteins can move into interstitial spaces (spaces between tissues);
- These fluids contain neutrophils, and possibly macrophages. A neutrophil is a type of granulocyte (white blood cell), it is filled with tiny sacs which contain enzymes that digest microorganisms. Macrophages are also a type of white blood cells that ingests foreign material.
- These fluids pool to form the bumps (weals). These can be surrounded by redness, called flares. And those are your lovely hives!
Klaus Ley, M.D., a scientist at the La Jolla Institute for Allergy & Immunology, reported in a study published in Nature that neutrophils are the human body's first line of defense; they are the main cells that protect us from bacterial infections. Their protective function is a positive one, however, they also have inflammatory properties that may eventually lead to heart disease and several autoimmune diseases, such as lupus. Effectively manipulating neutrophils is vital in disrupting inflammatory diseases.
So basically, it's an inflammation in response to what your body perceives as a potentially harmful intruder. Since there's no actual intruder here besides the cold weather, there's no way to remove the root cause. Therefore, the symptom should be treated. Antihistamines are generally prescribed for this problem.
How does hemp seed oil work on these processes?
I'm finding lots of studies that say that hemp seed oil is anti-inflammatory and antihistamine. I'm having trouble finding the exact mechanisms responsible... Together with the fatty acids (especially linoleic acid), the cannabinoid, cannabidiol, appears to be the key ingredient here. Humans have cannabinoid receptors (CB1 and CB2) in their skin. These are located on small and large nerve fibers running throughout the skin, even in the hair follicles. Human skin cells have the mechanism to bind, synthesize, and metabolize cannabinoids, although the role of this system is still contested. Booz (2011) and many other researchers argue that cannabidiol is a powerful antioxidant and anti-inflammatory. A deficiency in cannabinoid receptors results in mice increased swelling and recruitment of immune cells, so it is accepted that the cannabinoid receptors are factors in immune response.
Further research is ongoing.
Gamma linoleic acid has been shown in many studies to be anti-inflammatory. I've listed some of the studies below.
So that's why the hemp works. And it does work. It's pretty freakin amazing.
I just started a series on my Bohemia: Magical Textiles blog about prehistoric use of Cannabis sativa as a source of fiber and as an intoxicant. There's a lot of really interesting archaeological and documentary evidence. Have a look!
 |
| This gal. |
More studies
(from Speiser et al. 1999)PUFA supplementation influences the rate of biosynthesis of EFA derivatives as it seems to depend on the size of the precursors pool. Supplementing gamma linoleic acid (GLA) results in an increase of the less inflammatory PGE2. Similarly long chain omega-3 acids supplementation induces a marked reduction in LA and arachidonic acid (AA) in membrane lipids and also result in local generation of the less inflammatory PGE3.
Also, dihomo gamma linoleic acid (DGLA) is converted in the skin to PGE1, which is known to raise the levels of cAMP which in turn inhibits PLA2 (what’s PLA2) and so exerts anti-inflammatory effects by keeping AA locked into the phospholipidic membrane. Thus access of free AA to cyclo-oxygenase is denied and pro-inflammatory PG2 level is reduced. This implies the necessity of a well balanced mix of PUFA in the diet and in topical application.
PG2 is a powerful vasodilator and contributes to the characteristic edema related to inflammation. It must be noted that PG1 and PG3 are less pro-inflammatory. PGs are also immune modulators: PGE2 is a powerful inhibitor of cytotoxic T cells activity. In situ PG production happens simultaneously with UV erythema. Therefore omega-3 PUFA, by helping prevent PG2, has a photo-protective effect on skin.
Marshall, et. al. (Progr Lipid Res 1981 20 7312-734) demonstrate that nutritional balance between omega-3 and omega-6 EFA affects prostaglandin synthesis in the immune system improving certain skin inflammatory pathologies. This is due to the competitive inhibition of cyclo-oxygenase which does not release as much pro-inflammatory AA derived PG2, favoring the less active PG3. High LNA levels in the diet led to a decreased capacity for cyclo-oxygenase produced PGE syntheses in the thymus and spleen due to the preference of desaturase and elongase enzymes for the omega-3 EFA. This causes a larger decrease in AA than may be expected on the basis of dietary LA/LNA ratio.
Finally, Ziboh (Arch. Dermatol. 1989 125 241-245) has studied the accumulation in psoriasis lesions of leukotriene B4, the major pro-inflammatory metabolite of AA. He proved that GLA and EPA present in fish oil are potent inhibitors of leukotriene B4 generation. They seem to work by competitive inhibition of 5 lipoxygenase.
PUFA Metabolism in the Skin
The enzymes involved in PUFA metabolism are crucial. Unfortunately, the key enzyme, Æ6 desaturase enzymes and cannot convert LA to GLA nor DGLA to AA, but it can convert GLA to DGLA. The epidermis is therefore dependent on the continual formation of GLA and AA by the liver and on the transport to the skin by the blood.
Kassis et. al. (Arch. Dermatol. Res. 1983 275 9-13) proved that a person’s capacity to convert LA to GLA decreases with age, as do the levels of PGE1. Æ6 desaturase is inhibited by many exogenous factors such as diet, stress and aging. Therefore, a GLA deficit leads to: a lack of PG1, an off-balance PG1/PG2 ratio and various cutaneous problems related to aging, such as skin dryness, itching, erythema and skin thinning. A well-balanced oil has to be supplemented to counter this consequence of aging by circumventing the key Æ6 desaturase stage.
Benefits of Topical EFAs
Topical application studies proved that PUFA or preferably PUFA-rich vegetable oils (released by the skin esterase) are beneficial to the skin. Prottey et. al. (J. Invest. Dermatol. 1975 64 228-234) demonstrated that, after cutaneous application of sunflower seed oil, which is rich in LA, to the right forearm of EFAD volunteers for two weeks, the level of LA in their epidermal lipids was markedly increased, the rate of TEWL was significantly lowered and the scaly lesions had disappeared. No such changes were seen in the volunteers’ left forearms after cutaneous application of olive oil (containing nearly no LA).
Proksch et. al. (Br. J. Dermatol. 1993 128 473-482) demonstrated that disrupting the barrier function by topical acetone treatment results in an increase of free fatty acids, sphingolipids and cholesterol in the living layer of the epidermis, leading to barrier repair. DNA synthesis is also stimulated the same way as by occlusion. This is a possible second mechanism by which the epidermis repairs its barrier function of omega-6 PUFA limits DNA synthesis and helps restore the barrier function.
Coupland (Active Ingredient Conference Paris 1997 195-201) described how damaged or inflamed skin can be treated with oils containing GLA and SDA due to a reduction in inflammatory metabolites: PG. Photo-damaged skin may also benefit from these natural oils by inhibiting the secretion of TNF∝. Morganti et. al. (J. Appl. Cosm. 1985 3 211-222) showed that EFA application improves skin’s hydration capacity and protects aged skin against environmental insults. A cream containing 3% EFA prevents much better skin atrophy induced by a cortisone like compound which accelerates the skin’s aging process.
MIRI
