In the interests of full disclosure, scjas, do you have some financial connection with the promoters of parasitic therapies?
Just curious.
[QUOTE=SkipMagicI will say, however, Siam Sam, that claiming you have something worse to say about someone, but won’t because we’re not in the Pit, does little more than degrade the discussion. It’s probably better to either share your views in a new Pit thread, or just go along with the discussion without hinting at insults.[/QUOTE]
I was trying hard NOT to insult him, Skip, but I do apologize, to YOU, if I went a little too close to the line before.
You keep throwing out these statements off the top of your head, so you must have some figures to back them up. No doubt you’re well versed in all things Thai; I can’t imagine anyone asserting how many fall ill from what unless they know the figures.
As for the common cold, I have no idea myself how many catch it, but if the number did turn out to be more than have hookworm, it doesn’t mean that it beats out hookworm as a health problem. Temperatures drop to freezing up in the mountains of the North in the cold-season months; I’d guess there’s some colds there. But in the North, iodine deficiency is universally recognized as the No-1 health problem, but maybe they should do a head count and see who catches cold.
Or maybe instead of gibbering, someone needs to come up with some figures to back up their outlandish claims about Thai health problems.
Financial connection?
According to this, he (or someone coincidently :dubious: with the same web moniker) is the guy who founded Autoimmune Therapies.
First off, it does seem to work but it is new enough that it is not being done much, still has to have larger trials to prove it, and it will have to combat public perception. A good review was in a 2004 issue of Science (July 9). The article itself is firewalled in but here is an excerpt:
The idea considered precisely because societies with large parasitic burdens have little autoimmune disease burden. The belief is that the worm creates an anti-inflammatory state which protects it from attack, probably by effecting regulator T cells but perhaps also the inate immune system. The idea is to infect the patient with non-reproducing worms so as to minimize any adverse outcomes (although the cynic in me wonders if it isn’t really to just assure the need for regular redosing).
It turns out that indeed both atopy (allergies, asthma, eczema) and auto-immune diseases (Diabetes, Inflammatory Bowel diseases such as Crohn’s, Celiac, etc.) are much more common in societies that have greatly reduced the serious infectious disease and parasitic burden. The best explanation is that immune systems develop finesse with having survived serious insults (if they survive) and complex networks of mutually regulating responses. Without such experience immune systems can be klutzy and overreact in dysfunctional ways. On balance we are better off with decreased infectious disease rate but that benefit is offset some by these other diseases increasing. This is a societal effect, not a household one, but even at a household level it is documented. Want fewer allergies? Grow up on a farm exposed to animal poop and dirt with regularity. It also reduces your risk of developing JRA according to a recent Pediatrics article (2007, 120, pp 354-361). Or just get more viral infections in eraly childhood.
The op is correct. Some would, like Fry, rather live without worms even if they produced beneficial results. They’d rather deal with toxic medications.
This one is actually my field (as an immunologist specializing in inflammatory diseases), and short answer to this one is we don’t know. Personally, I believe in the hygiene hypothesis to a large extent. Not to say that it’s proven, but I’ve seen enough evidence, and it just makes enough sense. I wouldn’t publish with that as fact, but I do believe it to be true.
Second, there is some better than decent evidence that helminth infection could be therapeutic. This isn’t just urban legend or wishful thinking. There are actual studies and review articles (too many to cite, but a few):
All of these support the idea of helminths as therapeutic. As Dseid points out, this is relatively new data, so it’s not exactly in medical doctor’s tackle box, so it’s not surprising that people have not heard about it from their doctors. Doctors only get therapeutics after scientists identify them and test them. This one isn’t quite proven yet, and will require larger studies, but the evidence thus far is quite good.
Shorter answer, if I come down with Crohn’s tomorrow, this is without a doubt something I would look into.
Fair enough. I don’t personally see a problem with parasitic therapies (as I like to call them). After all, these creatures are the products of a billion or so years of evolution, while what we call modern pharmacology is 150 years old, tops. I was quite fascinated when I saw a news report about leeches being used in microsurgery (they can latch onto a blood vessel and keep it open with their anticoagulant saliva, giving a surgeon time to reattach severed fingers) and while I can picture intestinal worms having some positive effect, I’m not sure the associated negatives (not even counting the so-called ‘icky’ aspect) can be ignored.
In fact, the only thing I object to is the OP’s not-particularly-skilled sales pitch and the dishonesty within. Besides, it’s no more a “joke” that exposure to a bit of dirt helps your immune system than it’s a “joke” that lifting weights in a gym builds up muscle tissue.
Um, don’t you run the risk of E. Coli exposure with human feces? When even Dan Savage encourages caution around it, I’m inclined to be on the more prudent side as well.
Yes I do, I founded Autoimmune Therapies after putting my asthma into remission.
I am the guy who went to Cameroon to get hookworm, you can read my K5 post here:
So I know it works, not just because the research is so broad at this point but because I tested it on myself.
I have since been to Peru and Belize to obtain the better of the two species of hookworm, Necator Americanus.
I have also treated people through my business and the success rate tracks exactly to the what the research predicts.
This started as a simple question derived from the kind of irrational reaction I commonly see to this therapy. Everything I have quoted in defense of this approach has been third party science conducted by Universities, not drug companies.
My comparison of the common cold to HIV was just to illustrate the ridiculous statement that helminth infection was the number one health problem in S. Thailand. Helminths are usually benign, it is only when malnutrition is involved that they cause problems, or when the infection gets completely out of control.
My point was that just because 25% or whatever of a population has a helminth does not mean that any of them are sick.
The “dishonesty” would appear to be your posting of a “question” in a manner that appears to solicit business. If you would like to discuss the workings of or the reasons for your choice to allow yourself to be infected by parasites, I can see a possible legitimate discussion. However, this site is not to be used for solicitation, so if you have scientific support for your claims, stick to linking to sites with which you have no financial interest.
[ /Moderating ]
Thank you, scjas. As I think we’ve established, this technique may have some promise. (I am asthmatic, myself, and knew about it vaguely beforehand.) However, it’s one that’s still being researched. I don’t think many people would be honestly put off, if it was recommended by a doctor, but I think a lot of people really would prefer to let the general medical establishment conduct proper studies first, allow the results to percolate, and then take their … hm. I give the dog worming pills or deworming pills, it is the same result. Enworming pills? as prescribed.
In my original post I included links to my competitor, as well as to a non commercial site on which I originally wrote about my trip to Cameroon to infect myself with hookworm by walking around barefoot in open air latrines. Both were removed along with the link to my site. No problem, I suggested it when the original post was cited as spam. But if it were a straight solicitation why would I put my competitor’s link in, and above mine at that?
I am not here to drum up business, I have plenty, thanks. I am here to get an answer to my original question: why do people prefer terrible illness to doing something “icky”?
I know from personal experience that this works - I cured my asthma, and I have read dozens of peer reviewed scientific papers using double blind controlled studies that show that it works. I have cured my wife’s irritable bowel with this procedure, and my business partner has cured his psoriasis.
The question is, why is it so common for people who believe they are rational to so easily dismiss such evidence when they have so much at stake just because they find it repulsive to consider hosting intestinal worms?
That is a legitimate question and one worth an answer.
Fine, then give us some links to these studies.
In fact, had you started a thread in MPSIMS with just the study links and a “this is interesting, check it out”, you might have made a better first impression. I know I’m not impressed by the hamfisted approach of “are you too much of a wuss to face the TRUTH?!” That’s not an appeal to reason - it’s identical to the tack used by religious witnesses and conspiracy theorists.
NOTE: This message is too long to post all at once so I am going to break it up.
Sorry I got off on the wrong foot here, I genuinely am interested in the answer to my original question.
And I was not consciously taking the approach that anyone who did not agree with the idea that this works is a wuss, if that is what you mean by this post.
Nor am I saying that those who accept this therapy works but who refuse to even consider it when trying it has a good chance of curing their disease are wusses either.
What I was and am trying to say is “it sure is odd that faced with the alternatives of hosting few worms that have few if any side effects to cure their disease, or, allowing their disease to progress often leading to surgeries, degradation of quality of life and reduced life expectancy that so many refuse to even consider it because they find it disgusting”. To me that is ridiculous. It can be summarized as “I would die before having intestinal parasites”, which in some cases will be exactly what happens.
Links to studies or articles referencing studies:
Links to Media Reports
Medical News Today: Medical and health information
Nice paper with good epidemiology and summary of the hygiene hypothesis: Medical News Today
Tufts University, a great summary of the idea: Tufts University Alumni Magazine
An article from a British newspaper: Guardian-Observer online edition
A BBC article: BBC News
An Australian news site:
Publication unknown
And one from New Zealand: The Listener
One regarding MS and the Hygiene Hypothesis: Science Daily
I will post extracts for the research papers (a small subset of what is out there) in the next post.
**Research Papers **(membership often required to read anymore than the extract or summary, membership sometimes available for free) So, I saved you the trouble and have copied and pasted the publicly available extracts and summaries here. You can get to the full text by getting membership in the following medical and scientific journals and using the titles referenced below to search for the particular paper:
The Lancet, The British Medical Journal, The New England Journal of Medicine, etc.
1. J. Leonardi-Bee, D. Pritchard and J. Britton. Asthma and current intestinal parasite infection: systematic review and meta-analysis, Am. J. Respir. Crit. Care Med., 2006, 174(5), 514-23.
Abstract: RATIONALE: Epidemiologic studies suggest that intestinal parasite infections may protect against asthma. OBJECTIVES: A systematic review and meta-analysis of epidemiologic studies to determine whether total or species-specific current parasite infection is associated with a reduced risk of asthma or wheeze. METHODS: We searched MEDLINE, EMBASE, and CINAHL (up to January 2006); reviews; and reference lists from publications, with no language restrictions. We included studies that reported asthma or wheeze as an outcome measure and ascertained parasite infection by fecal examination. We estimated pooled odds ratios (OR) and 95% confidence intervals (CI) using data extracted from published papers, or where available, original data provided by authors, using random effect models. MEASUREMENTS AND MAIN RESULTS: Thirty-three studies met the inclusion criteria. Infection with any parasite was associated with a small, nonsignificant increase in asthma risk (OR, 1.24; 95% CI, 0.98-1.57; 29 studies). In species-specific analysis, Ascaris lumbricoides was associated with significantly increased odds of asthma (OR, 1.34; 95% CI, 1.05-1.71; 20 studies), while hookworm infection was associated with a significantly strong reduction (OR, 0.50; 95% CI, 0.28-0.90; 9 studies) that was directly and significantly related to infection intensity (p < 0.001; OR for highest tertile of infection, 0.34; 95% CI, 0.19-0.62). Other species had no significant effects on asthma. Infection effects on wheeze were derived from smaller numbers, but revealed a broadly similar pattern of results.
2. S. Scrivener, H. Yemaneberhan, M. Zebenigus, D. Tilahun, S. Girma, S. Ali, P. McElroy, A. Woodcock, D. Pritchard, A. Venn and J. Britton, Independent Effects of intestinal parasites infection and domestic allergen exposure on risk of wheeze in Ethiopia: a nested case-control study, Lancet. 2011, 3:358 (9292), 1493-9
Abstract: Why asthma is rare in rural subsistence societies is not clear. We tested the hypotheses that the risk of asthma is reduced by intestinal parasites or hepatitis A infection, and increased by exposure to dust-mite allergen or organophosphorus insecticides in urban and rural areas of Jimma, Ethiopia. METHODS: From 12876 individuals who took part in a study of asthma and atopy in urban and rural Jimma in 1996, we identified all who reported wheeze in the previous 12 months, and a random subsample of controls. In 1999, we assessed parasites in faecal samples, Der p 1 levels in bedding, hepatitis A antibodies, serum cholinesterase (a marker of organophosphorus exposure), total and specific serum IgE, and skin sensitisation to Dermatophagoides pteronyssinus in 205 cases and 399 controls aged over 16 years. The effects of parasitosis, Der p 1 level, hepatitis A seropositivity, and cholinesterase concentration on risk of wheeze, and the role of IgE and skin sensitisation in these associations, were analysed by multiple logistic regression. FINDINGS: The risk of wheeze was independently reduced by hookworm infection by an odds ratio of 0.48 (95% CI 0.24-0.93, p=0.03), increased in relation to Der p 1 level (odds ratio per quartile 1.26 [1.00-1.59], p=0.05), and was unrelated to hepatitis A seropositivity or cholinesterase concentration. In the urban population, D pteronyssinus skin sensitisation was more strongly related to wheeze (9.45 [5.03-17.75]) than in the rural areas (1.95 [0.58-6.61], p for interaction=0.017), where D pteronyssinus sensitisation was common, but unrelated to wheeze in the presence of high-intensity parasite infection. INTERPRETATION: High degrees of parasite infection might prevent asthma symptoms in atopic individuals.
**3. **P. J. Hotez, J. M. Hawdon, M. Cappello, B. F. Jones and D. Pritchard, Molecular Pathology of hookworm infection, Infect. Agents Dis., 1995, 4(2), 71-5.
Abstract: Within the past 2 years, progress has been made in the identification, isolation, and cDNA cloning of several macromolecules from hookworms. While the predicted amino acid sequences of some cDNAs resemble those from other nematodes, such as Caenorhabditis elegans, other cDNAs are unique to hookworms. Studies are under way to evaluate the function of these recombinant hookworm polypeptides with respect to the biology of hookworms in experimental animal models. The recombinant polypeptides are also under evaluation as vaccine targets and as natural products used in the treatment of human cardiovascular and autoimmune diseases.
**4. **K. Mortimer, A. Brown, J. Feary, C. Jagger, S. Lewis S, M. Antoniak, D. Pritchard and J. Britton. Dose-ranging study for trials for therapeutic infection with Necator Americanus in humans, Am. J. Trop. Med. Hyg., 2006, 75(5), 914-20.
Abstract: Epidemiological studies suggest that a hookworm infection producing 50 eggs/gram of feces may protect against asthma. We conducted a dose-ranging study to identify the dose of hookworm larvae necessary to achieve 50 eggs/gram of feces for therapeutic trials of asthma. Ten healthy subjects without asthma or airway hyperresponsiveness to inhaled methacholine received 10, 25, 50, or 100 Necator americanus larvae administered double blind to an area of skin on the arm. Subjects were seen weekly for 12 weeks and were then treated with mebendazole. Skin itching at the entry site and gastrointestinal symptoms were common at higher doses. Lung function did not change. Levels of blood eosinophils and IgE increased transiently, and levels of IgG increased progressively. All doses resulted in at least 50 eggs/gram of feces in the eight subjects who completed the study. Infection with 10 N. americanus larvae is well tolerated, elicits a modest host eosinophil response, and is potentially suitable for use in preliminary clinical therapeutic trials.
**5. **D. E. Elliott, R. W. Summers and J. V. Weinstock. Helminths and the modulation of mucosal inflammation, Curr. Opin. Gastroenterol., 2005, 21(1), 51-8.
Abstract: Inflammatory bowel disease is an emerging illness associated with socioeconomic development. The current epidemic of immune-mediated diseases may result from our loss of exposure to parasitic worms (helminths). This review summarizes some of the recent findings showing that helminths induce regulatory circuits that could prevent and treat inflammatory bowel disease. RECENT FINDINGS: Inflammatory bowel disease appears to result from a dysregulated immune response. Although genes influence the risk of inflammatory bowel disease, it seems that critical changes in our environment have permitted its expression. One such change is the eradication of helminths. Helminths can impede interleukin-12, interferon gamma, and tumor necrosis factor alpha release and promote interleukin-10, transforming growth factor beta, and regulatory T-cell production. Helminths can prevent and reverse intestinal inflammation in animal models of inflammatory bowel disease. In clinical studies of patients with inflammatory bowel disease, exposure to the helminth Trichuris suis reduces disease activity. SUMMARY: If harboring helminths protects against immune-mediated disease, then these animals must be viewed in a new light. Are there “good” helminths in addition to bad? Instead of being detestable objects marked for eradication, helminths should be viewed as useful animals that may produce important compounds helpful for therapy of human disease.
**6. **S. Ardizzone and G. Bianchi Porro. Biologic therapy for inflammatory bowel disease, Drugs, 2005, 65(16), 2253-86
Abstract: Despite all of the advances in our understanding of the pathophysiology of inflammatory bowel disease (IBD), we still do not know its cause. Some of the most recently available data are discussed in this review; however, this field is changing rapidly and it is increasingly becoming accepted that immunogenetics play an important role in the predisposition, modulation and perpetuation of IBD. The role of intestinal milieu, and enteric flora in particular, appears to be of greater significance than previously thought. This complex interplay of genetic, microbial and environmental factors culminates in a sustained activation of the mucosal immune and non-immune response, probably facilitated by defects in the intestinal epithelial barrier and mucosal immune system, resulting in active inflammation and tissue destruction. Under normal situations, the intestinal mucosa is in a state of ‘controlled’ inflammation regulated by a delicate balance of proinflammatory (tumour necrosis factor [TNF]-alpha, interferon [IFN]-gamma, interleukin [IL]-1, IL-6, IL-12) and anti-inflammatory cytokines (IL-4, IL-10, IL-11). The mucosal immune system is the central effector of intestinal inflammation and injury, with cytokines playing a central role in modulating inflammation. Cytokines may, therefore, be a logical target for IBD therapy using specific cytokine inhibitors. Biotechnology agents targeted against TNF, leukocyte adhesion, T-helper cell (T(h))-1 polarisation, T-cell activation or nuclear factor (NF)-kappaB, and other miscellaneous therapies are being evaluated as potential therapies for IBD. In this context, infliximab is currently the only biologic agent approved for the treatment of inflammatory and fistulising Crohn’s disease. Other anti-TNF biologic agents have emerged, including CDP 571, certolizumab pegol (CDP 870), etanercept, onercept and adalimumab. However, ongoing research continues to generate new biologic agents targeted at specific pathogenic mechanisms involved in the inflammatory process. Lymphocyte-endothelial interactions mediated by adhesion molecules are important in leukocyte migration and recruitment to sites of inflammation, and selective blockade of these adhesion molecules is a novel and promising strategy to treat Crohn’s disease. Therapeutic agents that inhibit leukocyte trafficking include natalizumab, MLN-02 and alicaforsen (ISIS 2302). Other agents being investigated for the treatment of Crohn’s disease include inhibitors of T-cell activation, peroxisome proliferator-activated receptors, proinflammatory cytokine receptors and T(h)1 polarisation, and growth hormone and growth factors. Agents being investigated for treatment of ulcerative colitis include many of those mentioned for Crohn’s disease. More controlled clinical trials are currently being conducted, exploring the safety and efficacy of old and new biologic agents, and the search certainly will open new and exciting perspectives on the development of therapies for IBD.
7. J. Kurtovic and I. Segal. Recent advances in biological therapy for inflammatory bowel disease. Trop. Gastroenterol., 2004, 25(1), 9-14.
Abstract: Immune system is a major determinant of pathophysiology of inflammatory bowel disease (IBD), and cytokines are well known mediators of immune system. Recently, informations on pro-inflammatory cytokines and their role in IBD have led to development of potential therapeutic approach to manipulate these cytokines and there by inhibiting inflammation in IBD. These therapeutic approaches include inhibitors of the tumour necrosis factor (TNF)-alpha lymphocyte trafficking, type 1 T helper (Th1) cell polarization and nuclear factor type beta; immunoregulatory cytokines and various growth factors. Studies on these therapies have documented variable results and the outcomes of many clinical trials are awaited. However, these potential therapies, if become real may revolutionise approach in patients with IBD. Analysis of the inflammed mucosa from patients with Crohn disease (CD) and ulcerative colitis (UC) have shown increased expression of certain proinflammatory cytokines such as interleukin-1 (IL-1), interleukin 6 (IL-6) and TNF-alpha. The latter is important in the recruitment of neutrophils into inflammed tissue, a process which results from three physiological steps: (i) rolling, (ii) adhesion, and (iii) transendothelial migration. Understanding of the biology of chronic inflammation has expanded the therapies available for IBD and particularly CD. At present, the biological therapies that are being used in clinical practice or investigated for the treatment of IBD are predominantly proteins, usually delivered intravenously or subcutaneously. The therapies used include: 1. TNF-alpha inhibitors: infliximab, CDP 571, etanercept, onercept, CNI- 1493 and thalidomide. 2. Inhibitors of lymphocyte trafficking: natalizumab, LPD-02 and ICAM-1. 3. Inhibitors of Th1 polarization: monoclonal antibodies for IL-12, interferon (IFN)-gamma and anti IFN-gamma. 4. Immunoregulatory cytokines: IL-10 and IL-11. 5.
**8. **J. Correale and M. Farez. Association between parasite infection and immune responses in multiple sclerosis, Ann. Neurol., 2007, 17.
Abstract: To assess whether parasite infection is correlated with a reduced number of exacerbations and altered immune reactivity in multiple sclerosis (MS). METHODS: A prospective, double-cohort study was performed to assess the clinical course and radiological findings in 12 MS patients presenting associated eosinophilia. All patients presented parasitic infections with positive stool specimens. In all parasite-infected MS patients, the eosinophilia was not present during the 2 previous years. Eosinophil counts were monitored at 3- to 6-month intervals. When counts became elevated, patients were enrolled in the study. Interleukin (IL)-4, IL-10, IL-12, transforming growth factor (TGF)-beta, and interferon-gamma production by myelin basic protein-specific peripheral blood mononuclear cells were studied using enzyme-linked immunospot (ELISPOT). FoxP3 and Smad7 expression were studied by reverse-transcriptase polymerase chain reaction. RESULTS: During a 4.6-year follow-up period, parasite-infected MS patients showed a significantly lower number of exacerbations, minimal variation in disability scores, as well as fewer magnetic resonance imaging changes when compared with uninfected MS patients. Furthermore, myelin basic protein-specific responses in peripheral blood showed a significant increase in IL-10 and TGF-beta and a decrease in IL-12 and interferon-gamma-secreting cells in infected MS patients compared with noninfected patients. Myelin basic protein-specific T cells cloned from infected subjects were characterized by the absence of IL-2 and IL-4 production, but high IL-10 and/or TGF-beta secretion, showing a cytokine profile similar to the T-cell subsets Tr1 and Th3. Moreover, cloning frequency of CD4(+)CD25(+) FoxP3(+) T cells was substantially increased in infected patients compared with uninfected MS subjects. Finally, Smad7 messenger RNA was not detected in T cells from infected MS patients secreting TGF-beta. INTERPRETATION: Increased production of IL-10 and TGF-beta, together with induction of CD25(+)CD4(+) FoxP3(+) T cells, suggests that regulatory T cells induced during parasite infections can alter the course of MS. Ann Neurol 2007.
Too long, didn’t read.
Just kidding.
My point of view and approach to this is that of someone who has spent hundreds or thousands of hours researching it, has travelled at great risk and expense to Cameroon, Peru and Belize in order to infect myself with hookworm. I have done so successfully twice, and each time I was able to cure my seasonal allergies and my asthma. I estimate that I and my partners have spent about $150K and the best part of three years doing this.
I know it works for me. I know from having read thousands of pages of research that it works for most who have Crohn’s, UC, Asthma and likely MS. That it is likely to work for type 1 diabetes, rheumatoid arthritis, migraine, psoriasis, scleraderma, fibromyalgia, lupus and other diseases because the mechanisms of those diseases are very similar to Crohn’s, asthma, etc. That is they are all caused by an awry inflammatory response.
I am not some quack or dopey headed wishful thinker who dresses in purple and wears crystals. I have personal experience and yards of scientific writing to back me up. So when someone, on the basis of nothing other than a cursory reading of my post and without any deeper looking into the links or research I cite calls me a charlatan or an idiot I get pissed off.
On the other hand if I had lead with the research I have just posted how many of you would have slogged through it? Just about zero I would bet.
Out of the experiences I have had promoting this therapy on disease forums I know that about a third to forty percent of the population will not even consider this approach, no matter what the facts.
This is disturbing. They vote after all.
These people have the attitude, “I know what I know, don’t bother me with facts”.
I find that strange, hence my original question.
As to whether or not I was trying to promote anything here, be serious. Why post a promotional message here when there are dozens of boards devoted to the sufferers of Crohn’s, Asthma and MS who consist of 100% of my target audience? i put the links to my site and to my competitor’s because they were easy places for this thread’s readers to go to get information, just like the wikipedia entry.
thanks
Again, thanks for exposing us to this, scjas.
… yeah, I meant to say that. Bookmarked, will read at length at work tomorrow.
Fair enough; I lack the scientific training to determine whether your cites are good or bad. However, I will be meeting later this month with rheumatologist Dr. Robert W. Simms, one of the world’s leading researchers on the study of scleroderma at Boston University School of Medicine. I will ask him what he thinks about helminthic therapy as a treatment for scleroderma, which my wife was diagnosed with a year and a half ago. I will report his professional opinion here. Would that be a satisfactory critique of your personal research that you could accept, good or bad, without getting pissed off?
ETA: If you would like to email me any links to websites, articles or research that you have, I will present it to him. My email address is in my profile.