Neurogenic Inflammation

Some quick info about Neurogenic inflammation and possible treatment options that are being explored. One thing I thought was interesting was UV lights effect on it. Seems I keep finding one common herb when researching neurogenic inflammation and that is Cayenne. It is too bad I had a horrible shed on cayenne and had to stop. However, that was at a high dose and CS has stated that doses as small as 6mg were used. Maybe the key is regulating the dosage to the proper amount. Enough to experience some of the benefits w/o any of the negatives that some can experience.

I guess overall the best way to reduce neurogenic inflammation would be to reduce stress. I've been gaining ground here so hope that helps.

Capsaicin and other naturally occurring compounds

The neurotoxin capsaicin depletes sensory nerves from neuropeptides and activates TRPVs, particularly TRPV1 (Steinhoff et al., 2003). TRP ion channels are promising targets for the treatment of itch. Topical application of capsaicin (0.075%) to deplete SP from cutaneous nerve terminals also activates the TRPV1 and alters follicular innervation (Figure 3b). The initial burning pain and hyperalgesia pose a challenging task in the initial management of patient compliance. Once this is overcome, however, the extended treatment with topical capsaicin leads to a dose-dependent, partially reversible (Simone et al., 1998) loss of epidermal C-fibers, which may relieve localized chronic itch (Figure 3b) without major side effects such as histamine-release or local edema (Steinhoff et al., 2003). By contrast, menthol activates the cold-sensitive TRPM8 and the resulting cooling perception can relieve the itch perception as well. The potential of new topical formulations containing natural compounds such as cinnamon oil, wintergreen oil, clove oil, mustard oil, and ginger that all activate TRPA1 may hold great promise.

UV-light triggers neuropeptide-release

There is evidence that UV exposure of skin reduces endothelial NK1-expres​sion(Staniek et al., 1998), induces epidermal hyperinnervation and triggers SP and CGRP-release from sensory nerves (Scholzen et al., 1999). In addition, UV-induced CGRP-release triggers tumor necrosis factor-alpha-release from mast cells (Seiffert and Granstein, 2002) and upregulates NEP expression in melanocytes and endothelial cells (Scholzen and Luger, 2004). In the wake of these events, UV-released neuropeptides may first add to UV-induced acute inflammation but ultimately induce immunosuppression via the above-described pathways. This response is possibly under the control of NGF (Scholzen et al., 1999; Seiffert and Granstein, 2002). The widely used anti-inflammatory effects of UV-light may therefore be contributed at least in part to UV-triggered neuropeptide-release as this evidently reduces, for example, cutaneous contact hypersensitivity responses (Seiffert and Granstein, 2002). Likewise, UV-induced proteases by reducing SP bioactivity may be beneficial for hyperproliferative skin diseases such as psoriasis, which is characterized by an increased immunoreactivity of SP-positive nerve fibers (Chan et al., 1997).

Neurokinin antagonists

As SP via NK1 acts both proinflammatory and immune-stimulatory, NK1 receptors are attractive pharmacologic targets to neutralize neurogenic inflammation. In modern clinical praxis, they serve as an important adjuvant strategy for the management of skin diseases such as atopic dermatitis, psoriasis or allergic contact dermatitis (Scholzen et al., 1998; Niizeki et al., 1999; Steinhoff et al., 2003). NK1 antagonist treatment is suited to reduce "danger-signaling" in the skin and thereby attenuate stress-induced aggravation of cutaneous inflammation T-cell mediated skin diseases as discussed above. NK1 antagonists have passed clinical trials and are now available for treatment of anxiety, nausea, and depression as well as pain (Steinhoff et al., 2003) and NK1 antagonist can be successfully delivered into the skin (Kikwai et al., 2004).

CGRP-receptor antagonists

CGRP and associated molecules are powerful tools to suppress antigen presentation, and may therefore find a place in the treatment of allergic and autoimmune skin diseases. Accordingly, novel non-peptide CGRP receptor antagonists such as BIBN4096BS, which are currently on trials for the treatment of migraine, appear to attenuate CGRP and AM-induced cutaneous microvascular responses. Future clinical dermatological research should therefore employ these antagonist alone ore in combination with neurokinin antagonists to neutralize neurogenic inflammation (Brain and Grant, 2004; Grant et al., 2005) or to attenuate CGRP-mediated tumor-induced hyperalgesia (Wacnik et al., 2005).

Neuropeptide degrading enzymes

Regulation of neuropeptide-degrading enzymes may have a powerful impact on the outcome of cutaneous inflammatory responses. A downregulation of endogenous proteases was observed in response to microbial infection (Rempel and Pulliam, 2005), which might aid to initialize the inflammatory response and to maintain accessibility of cells to cell-survival ensuring growth factors (Scholzen and Luger, 2004). Thus, targeting neuropeptide-degrading enzymes could be a therapeutic strategy for the treatment of inflammatory skin disease. However, increased NEP expression during lymphocyte maturation either marks immature cells or cells sentenced to apoptotic cell death (Scholzen and Luger, 2004). Moreover, since enhanced neuropeptide degradation may interfere with host defense, fine-tuning of this interventional strategy will be challenging.

Neuroimmunophilin ligands

Topical neuroimmunophilin ligand FK506 is widely appreciated in the therapy of chronic cutaneous inflammatory diseases, particularly of atopic dermatitis. Interestingly, besides its well-known immunmodulatory functions relying on calcineurin inhibition, FK506 also stabilizes cutaneous innervation and mast cells, and is capable of decreasing the number of nerve fiber-mast cell contacts in atopic dermatitis skin. The anti-inflammatory effects of immunophilin ligands may thus in part derive from their neuroprotective capacities. This is further supported by the observation, that FK506 as well as topically applied neuroimmunophilin ligand analogs (GPI1046 and GPI1511; Guilford Pharmaceuticals, Baltimore, MD), that lack its immunosuppressant activity, induce hair growth in mice. This suggests that the neuro-protective component of immunophillin ligand signaling plays a dominant role in cutaneous tissue remodeling processes as occurring during hair growth and potentially in neurogenic inflammation.

Does Resvestarol/Curcumin not work on a similar principle?

I tried cayene and all i had was a burning stomach and digestion!

is revestarol/curcmin an alternatrive to fin?

does cayene have to be takin with soy isoflavons

I believe you are right. I think I remember CS saying the Curc/Resv works in a similar manner but couldn't find it or at least saying that it specifically inhibits Substance P.

LLLT uses in reducing Neurogenic inflammation.

Phototherapy has been shown to affect cellular activity in the following ways: stimulate cell growth; increase cell metabolism; improve cell regeneration; produce an anti-inflammatory response; produce an edema reduction; reduce fibrous tissue formation; stimulate nerve function; reduce the production of substance P; stimulate long-term production of nitric oxide; decrease the formation of bradikynin, histamine and acetylcholine; and stimulate the production of endorphins.5 These photobiological responses largely are responsible for the pain-relieving effects often observed in patients treated with phototherapy.

The most dramatic examples include the different effects of LLLT irradiation on healthy tissue, inflamed tissue, and malignant tissue. Healthy tissue does not contain a Page 4 high concentration of biologically active chromophores (e.g., biogenic amine, histamine, serotonin, VIP, substance P) while inflamed tissue does. LLLT can mitigate the inflammatory response by stabilizing mononuclear phagocytic cells, stimulating leukocyte chemotaxsis, and preventing mast cell degranulation. This prevents the release of histamine, and other biogenic amines, which cause the cellular infiltration responsible for the four cardinal signs of inflammation: redness, heat, pain, and swelling. LLLT dampens the inflammatory cascade, mitigates inflammation, and allows first intention healing. Similarly, malignant tissue is defined by its high mitotic index, which supports the rapid, uncontrolled growth of cancer. Mitotic cells appear insensitive to LLLT irradiation while injured and dormant cells can be stimulated to divide.

Reducing Inflammation
by David Seaman, DC, MS, DABCN

Staying Healthy During Tough Economic Times

Many of us are feeling the economic crunch. Money is tight and the bills continue to arrive in our mailboxes. Stressful times like these demand resiliency on our part. Interestingly, a mentally stressed state can promote systemic inflammation.1-4 Avoiding mental stressors is not likely to be easy during these times, so we must consider the importance of avoiding systemic inflammation caused by a lack of exercise and a poor diet.

Our mechanically oriented training leads us to view inflammation as a consequence of an identifiable physical injury. However, inflammation is more complex than this. We promote development of chronic, systemic subclinical inflammation by avoiding exercise and remaining sedentary.5-8 In other words, we can become chronically inflamed without physical injury. Not surprisingly, we should exercise daily to help prevent inflammation, and we must also modify our dietary habits.

Pro-Inflammatory Nutrition Is Expensive

Chronic, systemic subclinical inflammation is also promoted by subsisting on the average American diet, which is high in calories and low in fiber and nutrients. Approximately 80 percent of the calories consumed by Americans are derived from refined flour products, refined sugar, refined seed oils (concentrated source of omega-6 and trans fats) and fatty meat.9 It is now common knowledge that eating excess calories from sugar and fat leads to postprandial systemic inflammation,10 which is thought to function as in insidious promoter of heart disease, diabetes, osteoporosis, osteoarthritis, rheumatoid arthritis, Alzheimer’s disease, obesity, hypertension, asthma, depression, inflammatory bowel disease, psoriasis and cancer.7,9-12

Anti-Inflammatory Nutrition Is Inexpensive

Lean meat, fish, chicken, fruits, vegetables and nuts form the foundation of a diet that blunts a postprandial inflammatory response. This is referred to as an “anti-inflammatory diet.”10 Not surprisingly, this diet is recommended to help prevent the above-mentioned pro-inflammatory diseases, the treatment of which represents a massive drain on financial resources, both personally and for businesses.7,9-12

A common argument is, “I can’t afford to eat lots of fruits and vegetables,” or “Healthy foods are expensive.” I tend to strongly disagree with these arguments. A cup of coffee and a doughnut can cost up to $5. A bottle of 20 oz. soda costs more than $1. In contrast, a 5-pound bag of frozen carrots, broccoli and cauliflower costs $5 at Sam’s Club. A 1-pound container of pre-washed organic salad greens costs about $4. A large sweet potato that can be split between two meals costs about 75 cents. While certain nuts are very expensive (macadamias, for example), many are very reasonable. Lean meats, fish and chicken are reasonably priced and can be added to the vegetables and sweet potatoes. Fresh fruit remains very reasonable and should be one of the snacks of choice.

Dark chocolate is inexpensive and can be mixed with raw nuts and raisins for a great snack or dessert. I often melt a 50-calorie piece of dark chocolate with a little coconut oil and add some nuts and raisins. I place this combination on a piece of wax/freezer paper and place it into the freezer for about 10 minutes. My reward is an anti-inflammatory candy bar.

In short, it is not more expensive to eat anti-inflammatory, if one shops wisely. Certainly, preventing the expression of chronic disease will save countless dollars and heartaches associated with the accelerated morbidity and mortality associated with pro-inflammatory living. In short, we cannot afford to eat any other way but anti-inflammatory.

Inexpensive Supplements for Health Promotion

Unlike what I once thought, nutritional supplements typically do not function as substitutes for medications, particularly when inflammatory dietary habits are maintained. There is no supplement that will lower blood pressure as consistently as medications. No supplement can influence blood sugar like Metformin. While ginger and turmeric inhibit cyclo-oxygenase, it is not with the same power as nonsteroidal anti-inflammatory drugs.

The key really seems to involve the adoption of an anti-inflammatory diet and taking key supplements that support the reduction of inflammation and free-radical generation. The basic supplements include a multivitamin without iron, magnesium, fish oil and vitamin D.13-19

Fortunately, the basic four supplements mentioned above are reasonably priced. The cost is approximately $60 to $80 per month, which is less than $3 per day. If a patient can only afford one supplement, vitamin D seems like the best choice because research has demonstrated that vitamin D insufficiency is pandemic. The next best financial choice for a supplement would be a multivitamin/mineral without iron. After that fish oil should be added and finally magnesium. If a fifth supplement can be afforded, probiotics are the best choice as they have a strongly anti-inflammatory effect in the gut.

If money is not at issue, additional supplements should be considered, including coenzyme Q10, lipoic acid, acetyl-L-carnitine, ginger, turmeric and garlic. These supplements help to promote ATP synthesis and reduce free radicals and inflammation.

Conclusion

While finances are tight for many due to external economic forces, we can easily make this situation a lot worse by pursuing disease expression due to a pro-inflammatory lifestyle. Medical care for pro-inflammatory diseases is extremely expensive and generally preventable by adopting an anti-inflammatory diet that is no more expensive than one that is pro-inflammatory. Key supplements can be added based on financial ability.

We should consider that paying for expensive medical care will put most of us into debt even when economic times are good. So, it makes no sense to pursue disease and expensive medical care with a pro-inflammatory lifestyle when economic times are not so good. Share this information with your patients and let them know nutrition does not need to be compromised, even when the economy is down.

References

1. Black PH, Garbutt LD. Stress, inflammation and cardiovascular disease. J Psychosom Res 2002;52(1):1-23.
2. Black PH. Stress and the inflammatory response: a review of neurogenic inflammation. Brain Behav Immun 2002;16(6):622-53.
3. Black PH. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain Behav Immun 2003;17(5):350-64.
4. Black PH. The inflammatory consequences of psychologic stress: relationship to insulin resistance, obesity, atherosclerosis and diabetes mellitus, type II. Med Hypotheses 2006;67(4):879-91.
5. Oegema TR. Molecular basis of the interaction of inflammation and exercise: keep on walking!Arth Rheum 2007;56(10):3176-9.
6. You T, Berman DM, Ryan AS, Nicklas BJ. Effects of hypocaloric diet and exercise training on inflammation and adipocyte lipolysis in obese postmenopausal women. J Clin Endocrinol Metab 2004;89:1739-46.
7. Nicklas BJ, You T, Pahor M. Behavioral treatments for chronic systemic inflammation: effects of dietary weight loss and exercise training. Can Med Assoc J 2005;172(9):1199-209.
8. Tjonna AE, Lee SJ, Rognmo O, et al. Aerobic interval training versus continuous moderate exercise as a treatment for the metabolic syndrome. A pilot study. Circulation 2008;118(4):346-54.
9. Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution of the Western diet: Health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.
10. O’Keefe JH, Gheewala NM, O’Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol 2008;51(3):249-55.
11. Simopoulos AP. Omega-3 fatty acids inflammation and autoimmune diseases. J Am Coll Nutr 2002;21(6):495-505.
12. Franco OH et al. The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%. BMJ 2004;329:1447-50.
13. Seaman DR. A sports nutrition: a biochemical view of injury care and prevention. In: Hyde TE, Gengenbach MS, Eds. Conservative Management of Sports Injuries, 2nd ed. Boston: Jones and Bartlett; 2007: pp. 1067-92.
14. Seaman DR. Nutritional considerations in the treatment of soft tissue injuries. In: Hammer WI, Ed. Functional Soft-Tissue Examination and Treatment by Manual Methods, 3rd ed. Boston: Jones & Bartlett; 2007: pp. 717-34.
15. Seaman DR. Nutritional considerations for pain and inflammation. In: Liebenson CL, Ed. Rehabilitation of the Spine: A Practitioner’s Manual, 2nd ed. Baltimore: Williams & Wilkins; 2006: pp. 728-40.
16. Ames BN. The metabolic tune-up: metabolic harmony and disease prevention. J Nutr 2003;133(5 Suppl 1):1544-8.
17. Ames BN. Supplements and tuning up metabolism. J Nutr 2004;134(11):3164S-8S.
18. Ames BN. Increasing longevity by tuning up metabolism. To maximize human health and lifespan, scientists must abandon outdated models of micronutrients. EMBO Rep 2005;6:520-4.
19. Ames BN. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. PNAS 2006;103(47):17589-94.

How Diet Can Feed Inflammation, Pain, and Chronic Disease
by David Seaman, MS, DC, DACBN

Neurogenic inflammation is thought to be involved in the pathogenesis of numerous conditions, such as osteoarthritis, migraine, dental disease, pancreatitis, virus-associated respiratory infection, nonproductive cough, allergic rhinitis, asthma, chronic bronchitis, sarcoidosis, inflammatory bowel disease, rheumatoid arthritis, and painful conditions in general.1-7



The figure at right represents a simplified version of the neurogenic inflammatory process. Immediately upon injury, damaged cells release various chemical mediators, and thereafter, intact cells in the area of injury produce many more mediators. Each of these mediators has receptors on group IV afferent fibers, which leads to the excitation or inhibition of the sensory nerve fibers typically associated with nociception and pain. One outcome of such stimulation can be chronic inflammation, pain, and the expression of the many diseases mentioned earlier.

Not generally appreciated is that group IV afferents also function to restore local tissue homeostasis and healing.8 Group IV afferents merely respond to the local chemical environment. I should emphasize that it is a huge error in thinking to assume that nociceptors only function to create pain. Nociceptors are extremely diverse in nature. Indeed, world-famous pain researchers understand better than the rest that group IV are not pain fibers:

"A nociceptor is not born to be and to remain that kind of fellow for the rest of his life. It is a dynamic entity, shifting its properties under the influence of, and according to, the necessities of its environment." 9

Notice in the figure that group IV afferents release substance P and CGRP (calcitonin gene-related peptide), which serve to stimulate local tissue cells. At this point in the neurogenic inflammatory process, chronic pain and disease would not be present. This is because substance P and CGRP are not themselves responsible for driving inflammation. Indeed, substance P, in particular, is often mischaracterized as an inflammatory chemical.

The pain, disease or healing outcome from substance P/CGRP release seems to be determined by the pro-inflammatory or anti-inflammatory nature of the chemicals released by the local cells. Notice the long list of mediators that local cells release; some promote inflammation and the diseases mentioned earlier, while others reduce inflammation and promote tissue healing – and nearly all of the mediators are regulated by diet. In particular, the eicosanoids or autocoids are derived exclusively from the fatty acids we consume. The leukotrienes (LTB), prostaglandins (PGE), prostacylins (PGI), lipoxins, resolvins, docosatrienes, and thromboxanes (TXA) are derived from either omega-6 (n-6) or omega-3 (n-3) fatty acids.

Humans are supposed to consume a 1:1 ratio of n-6s to n-3s; however, we currently average about 10:1 to 30:1.10 Anything above 4:1 is thought to be pro-inflammatory; this is because an increased level of dietary n-6 fatty acids leads to an increased production and release of pro-inflammatory autocoids from local cells (LTB4, PGE2, PGI2, TXA2).10 The omega-6 fatty acids and their autocoids also facilitate the release of some of the other pro-inflammatory chemicals listed in the figure, such as serotonin (5-HT), histamine, interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF), and growth factors.10

After the pro-inflammatory mediators are released, they again stimulate the local group IV afferents, which respond by releasing more substance P/CGRP – and thus, the cycle continues. Taking NSAIDs can only temporarily inhibit the conversion of pro-inflammatory fatty acids into their respective pro-inflammatory autocoids. After NSAID levels drop, we are left with a 30:1 ratio of n-6s to n-3s, which perpetuates the chronic inflammation cycle. We use the terms "inflammation" and "neurogenic inflammation;" however, "diet-driven inflammation" is a term that more accurately characterizes the problem.

Patients need to be told that their diet can either feed the healing process or feed chronic inflammation and the disease process. Group IV afferents can be referred to as pain fibers when conversing with patients who suffer from pain, and so these patients should be told that their diet functions to feed the pain fibers, leading to seemingly endless chronic pain.

Patients also need to know that correcting n-6 imbalances is not something a doctor can do for a patient. Only the patient can reduce his or her consumption of n-6s and increase n-3s, and this requires a disciplined approach to diet and supplementation. For example, consider that only fruits, vegetables, and potatoes have n-6:n-3 ratios below 4:1. Most fish, grass-fed animals and wild game have ratios approximately 4:1 or better. Fats/oils with acceptable ratios or low levels of n-6s include butter, olive oil, and coconut oil.11-12

Grains, grain flours, peanuts, and seeds have ratios of 20:1 or greater. Soy has a ratio of 7:1. Potato chips are oiled with corn, sunflower, cottonseed, or safflower oil, and these oils have n-6:n-3 ratios that range from 70:1 to over 100:1.11-12 These seed oils and the many packaged foods that are literally "bathing" in these oils feed the inflammatory process.

We and our patients should eat almost exclusively those foods with proper n-6:n-3 ratios. However, in today's fast-paced and inflamed society, it is likely that we are all going to come up short of our goal. For this reason, we all need to be supplementing with at least 1 gram of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish oil.

References

1. Bonnet CS, Walsh DA. Osteoarthritis, angiogenesis and inflammation. Rheumatology 2005;44:7-16.
2. Waeber C, Moskowitz MA. Migraine as an inflammatory disorder. Neurology 2005;64(Suppl 2):S9-S15.
3. Spierings EL. Pathogenesis of the migraine attack. Clin J Pain 2003;19:255-62.
4. Lundy FT, Linden GJ. Neuropeptides and neurogenic mechanisms in oral and periodontal inflammation. Crit Rev Oral Biol Med 2004;15(2):82-98.
5. Liddle RA, Nathan JD. Neurogenic inflammation and pancreatitis. Pancreatology 2004;4:551-60.
6. O'Connor TM, O'Connell J, O'Brien DI, et al. The role of substance P in inflammatory disease. J Cell Physiol 2004;201:167-80.
7. Brack A, Rittner HL, Stein C. Neurogenic painful inflammation. Curr Opin Anaesthesiol 2004; 17:461-64.
8. Byers MR, Bonica JJ. Peripheral Pain Mechanisms and Nociceptor Plasticity. In: Loeser JD (editor). Bonica's Management of Pain, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001: p.26-72.
9. Schmidt RF, Schaible HG, Mefslinger K, et al. Silent and active nociceptors: structure, functions, and clinical implications. Proc 7th World Cong Pain. Prog Pain Res Manag, Vol 2. Seattle: IASP; 1994: p.213-264.
10. Simopoulos AP. Omega-3 fatty acids in health and chronic disease. Am J Clin Nutr 1999;70(suppl):560S-69S.
11. Enig Mg. Know Your Fats. Bethesda Press: Silver Spring (MD): Bethesda Press; 2000: p.115.
12. Cordain L. The Paleodiet. Hoboken: John Wiley & Sons; 2002.

great info, hapyman. Gonna try out LLLT blood irradiation soon.

hapyman wrote:I believe you are right. I think I remember CS saying the Curc/Resv works in a similar manner but couldn't find it or at least saying that it specifically inhibits Substance P.

http://www.hairloss-research.org/UpdateResveratrol11-07.html

hapyman - Thanks for that info!

Recently lund posted an older study on cayenne. When it came out it flew in the face of other studies.
Not only that, but its methodology involved cayenne literally being soaked in human hair follicles for a long period of time, not something that would necessarily occur just by ingesting it. The result however was devastation for hair growth and it scared me and everyone else who saw it.

http://ajp.amjpathol.org/cgi/reprint/166/4/985.pdf

Since that time (2005) other studies have come forward with conflicting results. Then recent findings that cayenne was a CB1 receptor blocker gave new hope that maybe cayenne had something positive to it. It was after all one of the first hair loss remedies I had ever heard of and it came from Jay Kordich (the Juiceman) who claimed it was responsible for him keeping his hair. He used it topically with (first soaked in Whisky for two weeks). This was circa 1993.

Also there was a study that showed topical cayenne improving the efficacy of Minoxidil.
It seems now that only a low dose of cayenne would work for some scenarios such as in one study showing use for alopecia areata.

Looking back at the study (link above) and given many people's negative experiences with internal use cayenne appears to be less than positive for hair growth.

The potentially negative effect is due to the Transient Vanilloid Receptor-1 agonist action. Note that Curcumin also has a TRPV1 agonist action.

In my recent personal experience I tried popping lots of cayenne during stressful situations, it did not prevent hair loss but if anything had possibly a negative effect. While the study shows clearly that increasing transient receptor
potential vanilloid-1 receptor (TRPV1) will have a negative effect on hair, it was not certain if ingesting it would also have this effect, since the study involved direct exposure to cayenne.

Personal experience at least in my case and others like The Natural show that Curcumin & Resveratrol work. But strangely, there are some similarities in action between cayenne and Curcumin/Resveratrol. Nothing beats trial and error.

This study explains the synergy with Curcumin & Resveratrol

http://www.ncbi.nlm.nih.gov/pubmed/19359525.

"Collectively, we suggest that trans-resveratrol and curcumin act as antagonists/inverse agonists at CB1 receptors at dietary relevant concentrations. Therefore, these polyphenols and their derivatives might be developed as novel, nontoxic CB1 therapeutics for obesity and/or drug dependence"

Here is information about CB1 receptors (endo- and exocannabinoids and their effect on hair growth)

http://www.fasebj.org/cgi/content/full/21/13/3534

The above link explains also that the negative effect of TRPV1 is completely nullified by blocking the CB1 Receptor. I could only surmise that Curcumin/Resveratrol does a much superior job to blocking CB1 than Cayenne.

Thanks CS but I am just following your lead. I found what you were saying in the thread about hairloss theory very interesting. Especially the part about neurogenic inflammation. A mixture of stress (physical & emotional), diet and perhaps genetics.

Seems sometimes we get stuck in a cycle of stress while we are losing our hair. It is a very hard topic for a lot of people to cope with it. I think us especially need a positive outlook even if it seems the deck is stacked against us.

Lately I've been excited to get my loss under control and now am focusing on maximizing regrowth. I attribute my success to the top 6, lllt and laser blood irradiation. I am doing a lot of things but these are the things that have made the most drastic difference.

For those interested I think LBI is something really to consider, especially if you have poor circulation. It is really cheap and easy to try too. All it takes is one or two laser diodes and a small cheap power supply. I've also seen commercial units being sold from japan for about 200 USD but you can make a homemade one for 20 USD.

One major change I have noticed since starting LBI is the increase in circulation. For example veins in my arms are much more pronounced and I haven't even had time to lift weights over the past month. My muscles feel more "pumped" too. Also most importantly the circulation to my scalp is slowly getting better where it was horrible before.

I tried to find more research specifically about LBI and neurogenic inflammation and so far I couldn't find any more than what JDP has posted in the past. I don't think it is too ridiculous to theorize that it may help with lpa levels since it has an effect on other cholesterol molecules and pathways.

Just the other day I started the enzyme and pauling protocol as I am hoping it will take me to the next level. The enzymes will help clear up fibrotic tissue quicker and the pauling protocol will manage my lpa levels and aid in repairing collagen structure.