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what a load of old b****x, in my time I've worked and trained with some world class athletes (not cycling) and none of them would attribute their success to cow colostrum- genetics first and foremost, training second, vision and mental attributes next. All a bit of snake oil peddling if you ask me- Steve Peat's favourite supplements are Stella Artois and curry (info courtesy of his blog).Says it all in my book!
[img] http://www.sodahead.com/entertainment/should-taylor-lautner-remain-shirtless/blog-296528/ [/img]
Milkman's digging a bigger hole for himself!
[Edit]Damn that photo thing didnt work. This science thing is just beyond me!
I can see where everybody is coming from with their objections (and that is fair enough) but forget about Milkman for a moment (although he is being much nicer now- I think he just got overly defensive at the beginning)-
anyway, many of you are now being unfair to the scientists and their work- some of them conduct research as their job- why not just read the articles for yourselves and make your own decisions (without resorting to insults)? Somebody was asking about controlled trials earlier- if you do a literature search (try PubMed, or even Google Scholar, and type "colostrum and exercise" as your search terms) on the topic you will see that most of the published research studies were in fact placebo controlled double blind trials (so they cannot be biased). Also, if you just read the Abstract then you will miss a lot of important information- you need to read the full articles.
Bulter 88, joined forum 26th October...posted in one topic only so far... fancy that....
MicArms - MemberBulter 88, joined forum 26th October...posted in one topic only so far... fancy that....
True- but this is just my opinion anyway (and all I am saying is make your own mind up). You don't have to if you don't want to but it is what I think!
butler -= the point is that all the research Milkman quoted (that I could be bothered to read) does not show what he claimed it did.
The particular bit I looked at was his outlandish claim to cure heatstroke. Lots of research showing exercise and rise in body core temp causes gut issues. Nothing about his nostrum doing anything about this and anyway it would be a treatment for one symptom of heatstroke.
To say as he did that gut issues cause heatstroke is just absurd.
I suggest you drop it
Point taken on what you say about heatstroke vs one symptom TandemJeremy
Re: "I drop it"- all I was suggesting is that people read the information or research studies and make their own mind up. I don't think we need to get into an argument- you have clearly read the necessary information and made you own mind up... no?
Rocky Robin - MemberSteve Peat's favourite supplements are Stella Artois and curry (info courtesy of his blog).Says it all in my book!
🙂 apparently curry is good for you
Another shill.
I think its time the mods too action against them.
Wow..just spent 15 minutes of post-apprentice time reading through this....don't know what to say...pass the red wine Mrs Rock, I'm sure it thins the blood!
Shill- no no no TJ
Thought it would be nice to chip in on the debate but think I'll just keep my opinions to myself in future
(can't believe this is still going on btw)
Noooooooooooooooooooooooooooooooooooo
Please forgive me 🙂
?
For starting this thread 😉
butler - your first post on this thread and you are the third person to join to post on this thread. forgive me for being a tad suspicious
OK- fair point TJ- well I'm certainly not a shill and I'm not pushing or floggind anything- hopefully you'll see that for yourself in time?
Butler88 - Hmm - are you a sports physiology researcher or similar by any chance?
No (I'm a student), but I have been a subject in those sort of studies before (not with colostrum, but with sports drinks etc).
tbh, you'd have to be pretty naieve (sp?) to think that getting your mates to pile into a thread on here and lend support would result in success.
(really wasn't going to post again):
TJ (et al) - don't just pick on colostrum (and its purveyor) - As I asked (a lifetime ago), when are you planning on "proving" with some proper trial refs that THG etc (even epo) improve top athletes' performance (better still, endurance athletes) ? No surrogate markers or extrapolation - actual performance gains.
or is your argument, by extension, that they're ineffective snake oil - in which case why bother with all the testing etc ?
Scaredypants:
Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans.
Wilkerson DP, Rittweger J, Berger NJ, Naish PF, Jones AM.
J Physiol. 2005 Oct 15;568(Pt 2):639-52. Epub 2005 Aug 4.
Abstract
We hypothesized that 4 weeks of recombinant human erythropoietin (RhEPO) treatment would result in a significant increase in haemoglobin concentration ([Hb]) and arterial blood O(2)-carrying capacity and that this would (1) increase peak pulmonary oxygen uptake during ramp incremental exercise, and (2) speed kinetics during 'severe'-, but not 'moderate'- or 'heavy'-intensity, step exercise. Fifteen subjects (mean +/- s.d. age 25 +/- 4 years) were randomly assigned to either an experimental group which received a weekly subcutaneous injection of RhEPO (150 IU kg(-1); n = 8), or a control group (CON) which received a weekly subcutaneous injection of sterile saline (10 ml; n = 7) as a placebo, for four weeks. The subjects and the principal researchers were both blind with respect to the group assignment. Before and after the intervention period, all subjects completed a ramp test for determination of the gas exchange threshold (GET) and , and a number of identical 'step' transitions from 'unloaded' cycling to work rates requiring 80% GET (moderate), 70% of the difference between the GET and (heavy), and 105% (severe) as determined from the initial ramp test. Pulmonary gas exchange was measured breath-by-breath. There were no significant differences between the RhEPO and CON groups for any of the measurements of interest ([Hb], kinetics) before the intervention. Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON. RhEPO had no significant effect on kinetics for moderate (Phase II time constant, from 28 +/- 8 to 28 +/- 7 s), heavy (from 37 +/- 12 to 35 +/- 11 s), or severe (from 33 +/- 15 to 35 +/- 15 s) step exercise. Our results indicate that enhancing blood O(2)-carrying capacity and thus the potential for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence kinetics, suggesting that the latter is principally regulated by intracellular (metabolic) factors, even during exercise where the requirement is greater than the , at least in young subjects performing upright cycle exercise.
Also:
Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans.
Burnley M, Roberts CL, Thatcher R, Doust JH, Jones AM.
Exp Physiol. 2006 May;91(3):499-509. Epub 2006 Jan 23.
Abstract
We hypothesized that the reduction of O2-carrying capacity caused by the withdrawal of approximately 450 ml blood would result in slower phase II O2 uptake (VO2) kinetics, a lower VO2peak and a reduced time to exhaustion during severe-intensity cycle exercise. Eleven healthy subjects (mean +/- S.D. age 23 +/- 6 years, body mass 77.2 +/- 11.0 kg) completed 'step' exercise tests from unloaded cycling to a severe-intensity work rate (80% of the difference between the predetermined gas exchange threshold and the VO2peak) on two occasions before, and 24 h following, the voluntary donation of approximately 450 ml blood. Oxygen uptake was measured breath-by-breath, and VO2 kinetics estimated using non-linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in VO2peak (pre: 3.79 +/- 0.64 versus post: 3.64 +/- 0.61 l min(-1); 95% CL: -0.04, - 0.27) and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85). However, the kinetic parameters of the fundamental VO2 response, including the phase II time constant (pre: 29 +/- 8 versus post: 30 +/- 6 s; 95% CL: 5, -3), were not altered by blood withdrawal. The magnitude of the VO2 slow component was significantly reduced following blood donation owing to the lower VO2peak attained. We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise.
Jon
p.s. I am not selling rhEPO or blood donations!
Paper 1. Not athletes? Were they even used to regular exercise, I wonder
*extrapolation using a surrogate for performaceOur results indicate that enhancing blood O(2)-carrying capacity and thus the [b]potential*[/b] for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence [b]kinetic$[/b]
$ kinetics ? I R Not an exercise physiologist - what id the implication of this being unaltered ?
I'm back on kinetics and its meaning (rather the significance of "no effect"). Besides, removing blood cells and seeing a reduction does not allow the assumption that supraphysiological levels are better, does it ?We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise
(or, to put it another way, what would TJ say if you were milkman and posted all that up, but swapped "colostrum" for "epo" ?)
Scardypants:
Paper 1:
Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON
Paper 2:
The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition
Are we agreed that these two interventions have opposite effects here?
Paper 1:
RhEPO treatment enhanced the peak but did not influence kinetics
(The 'peak' refers to VO2peak and simply, the kinetics are how quick you get to VO2peak)
Paper 2:
blood withdrawal resulted in significant reductions in VO2peak
Again, are we agreed with opposing effects here?
Paper 2:
and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85)
We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and [b]exercise tolerance[/b]
Paper 1:
So, as EPO has the opposing effect on the physiology, it is 'likely' that exercise tolerance would be enhanced, no?
Jon
Scardypants:
Also sorry, I forget to answer your first question
Not athletes? Were they even used to regular exercise, I wonder
I personally know a good number of the authors on these papers and I was a participant in paper 2 - all of the people used in these studies were used to regular exercise, a good proportion would be described as athletes, and some were 'well trained'. At the time, my first year as an undergraduate, I held a BCF elite XC racing licence.
I am an exercise physiologist, I am not endorsing any product and my PhD involves these VO2 kinetics, VO2max/peak/ and exercise tolerance. I have no external agenda, and I believe that EPO does work as it appears to enhance haemoglobin concentration, and VO2peak, by ~7% in almost everybody tested.
Jon
p.s. I hope I make a better argument than our Milkman, these questions are good as will be asked similar questions in my PhD viva examination in a few months.
could someone sum this thread up? getting a bit wordy..
rootes1;
Wierd cows milk based drink.
You may or may not die of heatstroke if you exercise without drinking it first.
In a nutshell - milkman makes wonder milk, foxyrider and TJ are organising the STW group-buy.
right..... should i can the daily pint of Sterilized Milk then? It makes nice tea you see... (though not as good as condensed milk)
Colostrum 'may' enhance recovery and immune function... which in turn might allow an athlete to train harder/longer/more often without illness... thereby by proxy may also lead to enhanced performance (although data to support these suggestions is limited at best).
labmonkey - why did they bugger about with loads of "measures" in the epo study while failing to address or report the key issue, ie performance ?
it's obvious to me that the more RBC/Hb in the blood, the greater the O2 carrying capacity of said blood but I need to see that this translates into performance
(I notice incidentally, we're only on epo - presumably no, or far far softer, data for the other banned substances then ? As acknowledged on p1 of this lot, case for epo [b]is[/b] probably clear and has a convincing rationale - though not [b]proven[/b] imo, at least on this thread)
Don't get me wrong, I don't use or want to use any of this shite and I've no interest in seeing no-hopers like me wasting money on colostrum or anything else. I am a bit perplexed by the lambasting of milkman & his product and calls for utterly unimpeachable evidence (blinded controlled trials with big numbers of athletes) in support, when I don't believe this can be achieved for dozens of drugs that wada and uci would have us believe are "cheat" drugs.
I'd also be surprised if loads of top athletes aren't using the stuff, with or without evidence. If the purported mechanism (reduction in minor infection rates and their subsequent effect on training as I understand the stuff above) is correct then it'll be virtually impossible to demonstrate, ever.
I can only speak for myself but milkman was making claims that clearly cannot be supported by the research he produced and he used loads of anecdote and endorsements as "proof" which it is not. He also made some ludicrous claims about heatstroke.
Scaredypants:
As acknowledged on p1 of this lot, case for epo is probably clear and has a convincing rationale - though not proven imo, at least on this thread
Taking a step back from Sport and Performance for a second;
EPO was developed as a drug to combat severe clinical anemia (and other red blood cell related 'issues/diseases' etc). The vast majority of the research into this drug was undertaken to determine whether it would increase red blood cell mass, haemoglobin concentration, haematocrit etc -this research is a resounding YES and so the drug is widely used within the medical world to treat such conditions.
'Cheats' in sport got hold of this evidence and decided to take it to enhance performance, as the evidence for its effecton the blood would suggest a likely ergogenic effect. The number of 'very good' (and maybe artificially enhanced) athletes (mainly cyclists) that have been caught for using EPO and its derivatives (NESP and CERA) suggest that it may well work pretty well.
As exercise physiologists, we are not too concerned as to whether EPO actually enhances performance [i]per se[/i] (I am not aware of a single paper that has tested that hypothesis) but we are interested into the mechanisms that determine exercise tolerance (in health and also in disease).
The research group that I work within (including the authors of these two papers) strongly believe that the interaction between the VO2 kinetics, VO2max and the 'anaerobic capacity' play a central role in determining exercise tolerance/performance.
The purpose of these two papers was to investigate the effects of altering haemoglobin of these measures, rather than performance itself.
Jon
Furthermore, it is unlikley that any real 'athletes' would agree to take EPO as part of a study, as a positive test would result in a two year ban.
Jon / (LM)
As exercise physiologists, we are not too concerned as to whether EPO actually enhances performance per se (I am not aware of a single paper that has tested that hypothesis) ..... Furthermore, it is unlikley that any real 'athletes' would agree to take EPO as part of a study, as a positive test would result in a two year ban.
Aye, that's my point really - people asking for scientifically rigorous testing of a "new" fad product is ludicrous and UNFAIR
Out of interest, in your 2nd study, were you blinded as to whether blood was actually taken from you (ie control grp cannulated but minimal blood removal)?
I'd guess (from the almost nothing I know) that VO2peak might be more dependent on psychology than VO2max is and I might not try as hard if I'd had blood removed. Intuitively I'd expect a fall, but always nice to see controls all the same ...
Aye, that's my point really - people asking for scientifically rigorous testing of a "new" fad product is ludicrous and UNFAIR
Hay - wait up - this was in response to the wildish claims made by Milkman. My OP indicated I did not believe the hype concerning how beneficial Bovine Colostrum is with intensive training NOT how it hasn't been researched enough yet. Then it has gone on to how Milkman is suggesting its a wonder supplement and spouting rubbish he did obviously not understand. If you make claims you should back it up not spouting stupid pseudo-science!
If you notice it seems his claims have been edited by EU directives!
http://www.neovite.com/benefits/Default.asp
This was my point - you cannot make claims if you can't prove them. We would have been happy if he suggested the potential benefits and they are researching them as we speak!!! And yes some of us have a biomedical research background too!
Oh god I said I wasn't going to get sucked in again 😯 🙁
just when i thought i was out...they pull me back in
Scaredypants:
I am quite enjoying this debate, thanks for the questions!
Aye, that's my point really - people asking for scientifically rigorous testing of a "new" fad product is ludicrous
People need to understand the EPO was not developed for sport, it was developed to treat a disease - therefore the evidence does not exist.
Milkmans marketing of his colostrum product suggests that it will be of use in sport and they appear to be selling it on that premise - therefore he needs to get research to directly support such claims.
Out of interest, in your 2nd study, were you blinded as to whether blood was actually taken from you (ie control grp cannulated but minimal blood removal)?
Nope, we all went down to the NHS blood donation service and did our bit for society... we knew that blood was being withdrawn, you could see it if you looked around a bit on the bed.
It would have been nice to have a control group that did not have blood withdrawn, but whether there was a (negative) placebo effect was not the focus of this work.
We have to trust our participants to go 'as hard as possible, for as long as possible' - we verbally encourage (shout at) then to give a maximal effort!
I'd guess (from the almost nothing I know) that VO2peak might be more dependent on psychology than VO2max is and I might not try as hard if I'd had blood removed.
VO2max and VO2peak are essentially the same thing, its the highest amount of oxygen consumed by the muscle in one minute. Differing methods of determination of this measure has given rise to the two names. I won't go into the detail here unless really prompted - or put Day et al 2003 into pubmed.com and you might find it yourselves.
Psychology is a factor in performance, there is no denying that, and as a physiologist, it pains me to accept that. Someone could intentially 'fake' exhaustion early and we would then get a lower VO2peak, yeah sure, we have to trust them not to do that. But, no will in the world can make you get a higher VO2max either, your body can only use so much oxygen - end of story.
Jon
foxy - my point is, what's your take on the claims that THG, testosterone etc help with intensive training ?
Foxyrider:
Oh god I said I wasn't going to get sucked in again
Sorry, I am avoiding the colostrum debate as much as possible.
Just answeing some questions on EPO / blood donation etc as someone appears interested in our work - this is rare in Science!
@ jon - VO2max is sort of incontrovertible, I thought (where the line forms a plateau). I thought VO2peak was the point at which subjects (most of us) don't reach plateau but it hurts too much to go on, hence more susceptible to psychology ?
foxy - my point is, what's your take on the claims that THG, testosterone etc help with intensive training ?
I don't care as its off my topic list!
Scaredypants:
my point is, what's your take on the claims that THG, testosterone etc help with intensive training?
This is my last post (hopefully) before I vanish (not literally) for the day...
For 'endurance exercise' i.e. that lasting more than about 2 mins, the most effective ergogenic aids/drugs are the ones that enhance either O2 delivery [i]to[/i] the muscle or those that facilitate O2 utilization [i]within[/i] the muscle - as oxygen and carbohydrate (and fats) are the principle providers of energy to the muscle to support exercise.
Jon
Scaredypants:
OK, one more... Day and collegues can explain this one!
VO2max is sort of incontrovertible, I thought (where the line forms a plateau). I thought VO2peak was the point at which subjects (most of us) don't reach plateau but it hurts too much to go on, hence more susceptible to psychology ?
J Appl Physiol. 2003 Nov;95(5):1901-7. Epub 2003 Jul 11.
The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.
Day JR, Rossiter HB, Coats EM, Skasick A, Whipp BJ.
Abstract
The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a "plateau"), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.
once you're back from work then 😉 :
For 'endurance exercise' i.e. that lasting more than about 2 mins, the most effective ergogenic aids/drugs are the ones that enhance either O2 delivery to the muscle or those that facilitate O2 utilization within the muscle - as oxygen and carbohydrate (and fats) are the principle providers of energy to the muscle to support exercise.
so which are they ?
any drugs to increase lactate tolerance in the shorter term (eg "sprinting" the last mile of a stage or a short TT) ?
and why did landis do that stoopid thing with testosterone ? (or did he re-dope with contaminated blood?)
Your milkman is back from the dairy
On Tuesday I posted literature showing the effect of heat stress on the performance of your gut barrier function. I have also illustrated that endoxemia can be measured by bacterial fragments from the gut, found in the bloodstream (LPS). Foxyrider claims he has an alternative theory of endotoxemia, but has yet to produce it. Please do.
Heat stress can be induced both exothermically, as in the laboratory study, or by intense exercise as illustrated in the Ashton study. Remember that the return blood-flow from the legs, where the heat is being generated, flows along the posterior vena cava right next to your small intestine, so it's no surprise that this is the hottest part.
Let me now introduce a further example of heat stress and the response on the mammalian gut, the design of which goes back to our common mammal ancestor. The only mammal capable of enduring high core temperatures is the camel. The pathway utilised by this species is to enhance the repair capacity of the gut in the form of increased IGF-1 production and a higher number if IGF-1 receptors in the surface tissue of the gut. Please consider the following study
Growth Factors. 2003 Sep-Dec;21(3-4):131-7.
Distribution of insulin like growth factor-1 (IGF-1) and its receptor in the intestines of the one-humped camel (Camelus dromedarius).
Al Haj Ali M, Mensah-Brown E, Chandranath SI, Adeghate E, Adem A.
Department of Pharmacology, UAE University, United Arab Emirates.
Abstract
The distribution of insulin-like growth factor-1 (IGF-1) and its receptor in the gut of the one-humped camel (Camelus dromedarius) were studied by immunohistochemistry and quantitative receptor autoradiography. IGF-1-IR cells occurred mainly in the lamina propria and epithelium of the small intestine, while in the large intestine positive cells were seen in the columnar cells of the epithelial layer of colonic glands. IGF-I was also discernible in the muscularis externa of the intestines. Autoradiography revealed a higher concentration of receptors in the mucosa compared to the muscular layer. With regard to the mucosa, the highest density of receptors was discernible in the duodenum. Immunohistochemistry revealed the main sites of the receptors to be the lamina propria, epithelia of the crypts and the villi of intestines. Double immunofluorescence studies with combined antisera to IGF-I and its receptor showed that the ligand and its receptor usually occurred within the same cell in the mucosa. A few cells with varied profiles immunoreacted to either the ligand or the receptor but not to both. Cells with varied profiles immunoreacted to antiserum of the receptors but not to the ligand in the muscle layer. Thus IGF-1 might be acting on its receptor via both an autocrine and paracrine modes in the camel mucosa. In the muscularis layer, IGF-1 may be acting by different mechanisms. Our data demonstrate that unlike all other mammals studied, the camel contains a high concentration of IGF-1 receptors in the duodenal mucosa compared to other parts of the camel gut. It also possesses a higher concentration of the receptor in its mucosa compared to the muscle layer. We speculate that this might be a significant feature necessary for the regenerative ability of the duodenal mucosa in the one-humped camel.
PMID: 14708941 [PubMed - indexed for MEDLINE]
So, for readers that have a science based education, the idea that a source of repair trigger proteins (IGF-1, EGF) other than from your own saliva can effect an improvement in the performance of your gut under conditions of heat stress must surely be getting clearer even to the most stubborn resisters and ranters. For those of you unfortunate not to have had the education of Foxyrider or Tandemjeremy I have shown a practical example of heat stress resilience in the Attenborough video showing human performance where humans are specifically adapted do dissipate our excess heat by being bare skinned, sweating over the whole area of the skin, reduced sun exposed surface area by standing vertically with an insulating heat protecting hair cover for the top of the head, with low energy two leg locomotion, compared with that of the much stronger faster Kudu which isn’t.
Let's look at some the consequences of the rants that started this thread. Kimber has stopped eating black pudding now that he knows it's made from ox-blood. Clubber is planning to make a fortune by harvesting the saliva that Kimber has become reluctant to swallow now that he's learned it's full of growth factors, and at a cheaper price than goat’s milk, camel’s milk or cow’s colostrum too. Seriously Kimber, you will have to swallow your saliva. If you don’t your small intestine may ulcerate leading to toxic shock and organ failure, not unlike heatstroke. There is plenty of research into this gut state where it has been induced by the tube feeding of comatose patients in intensive care but you’ll have to look this bit up for yourself.
There are studies showing a number of other ways of combating the problem but you’ll all have to be very good and apologise nicely before I'll tell you. One thing for free however, be careful if you use the Tony Ashton vitamin C method. A national Olympic road race squad used added vitamin C in their drinks to guard against heat stress permeability at the Beijing games. Unfortunately the coaches underestimated their actual hydration needs. They ended up with too much retained ascorbate, had a lot of excess fluid in their muscles to buffer it and suffered from a lot of cramps and had lousy results, or at least so I am informed by a reliable source. Call me if you want to know which country
Labrat may be pleased to know that his trip to hospital may have been one of the number leading to our first NHS trial planned with his local hospital for that very thing, post operative recovery.
Your claims to have a bullshit detector really do seem pretty thin. When was it last calibrated? Rather than my 40-year professional career, try initialising it with the credentials of our principle gastroenterology researcher - he is a Fellow of the Royal College of Physicians, the Royal College of Pathologists and the Academy of Medical Scientists and probably UK's most published author in this field. It’s a comfort to me to know that an eminent researcher is prepared to include a humble chap like your milkman as a co-author in spite of Foxyrider’s reservations. Here's a look at one of his studies where he uses colostrum to prevent permeability inducing gut damage caused by using non-steroidal anti-inflammatory drugs.
Clin Sci (Lond). 2001 Jun;100(6):627-33.
Co-administration of the health food supplement, bovine colostrum, reduces the acute non-steroidal anti-inflammatory drug-induced increase in intestinal permeability.
Playford RJ, MacDonald CE, Calnan DP, Floyd DN, Podas T, Johnson W, Wicks AC, Bashir O, Marchbank T.
Department of Gastroenterology, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London W120NN, UK. r.playford@ic.ac.uk
Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) are effective analgesics but cause gastrointestinal injury. Present prophylactic measures are suboptimal and novel therapies are required. Bovine colostrum is a cheap, readily available source of growth factors, which reduces gastrointestinal injury in rats and mice. We therefore examined whether spray-dried, defatted colostrum could reduce the rise in gut permeability (a non-invasive marker of intestinal injury) caused by NSAIDs in volunteers and patients taking NSAIDs for clinical reasons. Healthy male volunteers (n=7) participated in a randomized crossover trial comparing changes in gut permeability (lactulose/rhamnose ratios) before and after 5 days of 50 mg of indomethacin three times daily (tds) per oral with colostrum (125 ml, tds) or whey protein (control) co-administration. A second study examined the effect of colostral and control solutions (125 ml, tds for 7 days) on gut permeability in patients (n=15) taking a substantial, regular dose of an NSAID for clinical reasons. For both studies, there was a 2 week washout period between treatment arms. In volunteers, indomethacin caused a 3-fold increase in gut permeability in the control arm (lactulose/rhamnose ratio 0.36+/-0.07 prior to indomethacin and 1.17+/-0.25 on day 5, P<0.01), whereas no significant increase in permeability was seen when colostrum was co-administered. In patients taking long-term NSAID treatment, initial permeability ratios were low (0.13+/-0.02), despite continuing on the drug, and permeability was not influenced by co-administration of test solutions. These studies provide preliminary evidence that bovine colostrum, which is already currently available as an over-the-counter preparation, may provide a novel approach to the prevention of NSAID-induced gastrointestinal damage in humans.
PMID: 11352778 [PubMed - indexed for MEDLINE]
I really must thank the contribution of Rocky Robin, he really made my day -
“what a load of old b****x, in my time I've worked and trained with some world class athletes (not cycling) and none of them would attribute their success to cow colostrum- genetics first and foremost, training second, vision and mental attributes next. All a bit of snake oil peddling if you ask me- Steve Peat's favourite supplements are Stella Artois and curry (info courtesy of his blog).Says it all in my book! “
The very essence of rant. A perfect 10. “It can’t possibly be true because he hasn’t heard of it.” He may not have had the education of Tandemjeremy or Foxyrider but he’s certainly made of the same stuff.
A point where Robin and I will certainly agree is that you will need to train harder or smarter to become faster. We don’t sell colostrum on the basis that if you take it you don’t need to train. But if you increase your training load to the point where the physiology of your gut or immune system is challenged then you really should consider using it.
I would like to thank the more open minded members who have offered me their sympathy. I am not defensive however, I am indignant. The only consolation I can draw from these exchanges is that not one of the scientists here have picked up the phone to engage in a real world debate rather than posting snide remarks and anonymous sniping. Whatever happened to scientific curiosity.
[i]Whatever happened to scientific curiosity.[/i]
It was killed in the stw 'cut and paste' war of October 2010...
I think the problem is Milkman that no one is going to get you to change your mind - you have a business to run, even if someone on here said 'hang on mate what about ....' and it shot all your 'evidence' down in flames you'd still carry on because you have to.
It would be like trying to convionce a Jehovas witness on the doorstep that God doesn't exist - fun for a bit but ultimately pointless.
It may be that your product is suitable for use by certain elite athletes but for the average mtber the advantages (if there are any) are likely to be vanishingly small.
all in my opinion of course.