Hemp oil
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...This is taken from Medicalmarijuana.com. Visit the link for citations of studies.
Recent evidence has shown that cannabinoid receptors, CB1 and CB2 are expressed in healthy and diseased skin...The CB1 receptor is located on nerves that run through out skin; large nerves fibers and even small nerve fibers associated with hair follicles have the receptors. Furthermore, previous work has demonstrated that human skin cells, epidermal ketinocytes, have the machinery to “synthesize, bind, and metabolize anandamide (AEA).” While the role of the endocannabinoid system in skin is a bit of a mystery, it appears to be important in skin cell maturation.
Cannabinoids may attenuate allergic responses. Mice lacking cannabinoid receptors experience more swelling and recruitment of immune cells than normal or wild-type mice.Cannabinoids are present in hemp seed oil.
Composition of Hemp Seed Oil
Fatty Acids (% w/w)
Linoleic Acid 52-62
-Linolenic Acid 12-23
Oleic Acid 8-13
Palmitic Acid 5-7
Stearic Acid 1-2
-Linolenic Acid 3-4
Eicosanoic Acid 0.39-0.79
Eicosenoic Acid 0.51
Natural Products
Cannabidiol 10 mg/kg
9-tetrahydrocannabinol ** nd [up tp 50mg/kg in oils from unwashed seeds]
Myrcene nr 160 mg/L
-Caryophyllene nr 740 mg/L
-Sitosterol nr 100-148 g/L‡
-Tocopherol 7-80 ppm†,†† tr
-Tocopherol 710-870 ppm†,†† 468 mg
Studies!
Booz (2011) and many other researchers argue that cannabidiol is a powerful antioxidant and anti-inflammatory. Many studies have been done, but so far the mechanism remains somewhat of a mystery. Further research is ongoing.
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.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.
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.
Larregue (Prostaglandines et thromboxanes Masson 1997) reviewed the importance of prostaglandin (PG) in skin. PGs are not stored but are synthesized on request after being stimulated. PG2 are synthesized from AA present in cell membranes.
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.
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.
Sunflower oil
From Livestrong:Sunflower oil contains gamma linolenic acid, which is an omega-6 fatty acid. Such fatty acids are essential to hair health, says Spencer David Kobren in his book, "The Truth About Women's Hair Loss: What Really Works for Treating and Preventing Thinning Hair." GLA also is effective in preventing hair loss from male and female pattern baldness as well as alopecia areata, which causes round patches of lost hair. Just 1 tsp. a day is all that's needed, Kobren says.
Coconut oil
A study by Rele AS and Mohile RB suggests that coconut oil is very effective in preventing protein loss from hair. This means that hair does not weaken and break as much.
Previously published results showed that both in vitro and in vivo coconut oil (CNO) treatments prevented combing damage of various hair types... Among three oils (coconut, sunflower, mineral), coconut oil was the only oil found to reduce the protein loss remarkably for both undamaged and damaged hair when used as a pre-wash and post-wash grooming product. Both sunflower and mineral oils do not help at all in reducing the protein loss from hair.
This difference in results could arise from the composition of each of these oils. Coconut oil, being a triglyceride of lauric acid (principal fatty acid), has a high affinity for hair proteins and, because of its low molecular weight and straight linear chain, is able to penetrate inside the hair shaft. Mineral oil, being a hydrocarbon, has no affinity for proteins and therefore is not able to penetrate and yield better results. In the case of sunflower oil, although it is a triglyceride of linoleic acid, because of its bulky structure due to the presence of double bonds, it does not penetrate the fiber, consequently resulting in no favorable impact on protein loss.
Palm oil
Contains Vitamins A, E, and beta-carotene. Anecdotal evidence promotes this oil as a good hair moisturizer and hair fall preventative. I've also seen stories negating those claims.Unfortunately, according to Treehugger.com, palm oil harvesting causes enormous damage to wildlife habitat. The article quotes Glen Horowitz's article in the LA Times:
"Whether it's used as an additive in soap, cosmetics or food, or processed into a biofuel, palm oil is one of the worst culprits in the climate crisis. Most of it comes from the disappearing, ultra-carbon-rich rain forests of Indonesia and Malaysia, of which a whopping 25,000 square miles have been cleared and burned to make way for palm oil plantations.
That burning releases enough carbon dioxide into the air to rank Indonesia as the No. 3 such polluter in the world. It also destroys the last remaining habitat for orangutans, Sumatran rhinos, tigers and other endangered wildlife."
Jojoba oil
Supposed to work together with sebum, is antibacterial and anti-inflammatory. According to the Journal of Cosmetic Dermatology, jojoba oil helps hydrate and remove gluey remnants from your hair.The linoleic acid content is 5%, and the oleic acid content is 5-15 %. Oleic acid thickens the sebum, so I wouldn't put jojoba oil directly on my scalp.
Castor bean oil
Supposed to help hair growth and texture, although no studies have been done to prove this. Antibacterial and antifungal properties. Contains ricinoleic acid, a type of fatty acid shown to possess anti-inflammatory properties.Virgin shea butter
She butter is very well trusted for hair and has been used in Africa for centuries to treat dry, curly hair. Contains Vitamins A and E, moisturizes scalp and hair, improves strength and elasticity of the hair shaftAverages 6% linoleic acid and 46.4% oleic acid. Again, I wouldn't put this directly on my scalp as it could exacerbate my thick sebum issues.
I've seen studies on its efficacy as a skin-care product, but have not been able to find one on hair and scalp issues. The studies were all positive for collagen replacement, moisturizing benefits, and wound healing. Lots of positive anecdotal evidence, and almost no negative for hair care use.
Tamanu Oil
Comedogenicity Rating: 2
Miri
