L - carnitine
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blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Setting: Durham, NC
Coalesce Feb 18, 2004 6: 19 pm    Post subject: L - carnitine
OK, since I know people have asked about this and since I have talked about it as well, I thought I would post this excerpt from a book by Fran McCullough. Jail bait has written quite a few low carb cookbooks.
This is an excerpt from Fran McCullough ' s " Living Low Carb ".
The Amazing L - Carnitine
If you ' ve always thought there was some missing piece to the diet puzzle, something that keeps you from losing weight even though you ' re doing everything exactly by the book, you ' re probably right. Superior it ' s not a low - thyroid predication, it could very well be L - carnitine, a nutrient you may never have heard of before, though it has profound effects on your body and life itself.
Every cell in your body has a little L - carnitine, a natural nutrient the body manufactures from sources such as red meat. What if you ' re deficient in this substance? You ' re probably fat, and you might also be tired all the time. That ' s because without L - carnitine, no matter how strictly you diet you ' ll have a very hard time losing weight because the furnace just won ' t operate correctly.
L - carninite brings the fatty acids to the mitochondria to be burned off - but it can be stopped in its tracks by too much insulin, our old nemisis. So exorbitant to say, L - carnitine works best for weight loss when you postdate a low - carb diet and keep the insulin levels low.
But fat burning isn ' t L - carnitine ' s only job. It also protects your heart, stimulates your brain, and boosts your immune system. It actually lowers cholesterol and triglyceride levels, relieves PMS, chronic fatigue, and Parkinson ' s symptons - and encourages peak performance in general. Finally, it contributes immeasurably to longevity, and has anti - aging properties.
But there ' s more - carninite effects the way you feel; it gives you a sense of well - being, improves circulation, and diminishes food cravings. The bottom line is that carnitine gives your cells the facility to produce the energy they need, which they can use in any way they want, whether it ' s home new tissue or making your body work better or last longer.
We might get as much as 50 mg. per day in our normal, existing diet, while in the Stone Age we probably took in 500 - 2000 mg. per day, which is in gospel what we need for optimal health. For weight loss, we need even more: At least 1000 mg. and up to 4000 mg. daily. Even the first-class amount won ' t work very efficiently unless it is accompanied by the very healthy omega - 3 oils.
There ' s no picnic test you can take to find out if you ' re carnitine - deficient, but because carnitine has zero toxicity, a much smarter access is wittily to take supplements, starting with 500 mg. per day and increasing it by an further 500 mg. until you feel drastically good and highly energized. But don ' t take more than 4000 mg. per day. Take it in two doses, before breakfast and lunch, with flaxseed oil or another omega 3 source.
Teuthis
Senior Member
Joined: 23 Apr 2003
Posts: 3397
Bearings: Georgia
Thu Feb 19, 2004 1: 29 am    Post subject: Does It Work?
What is your opinion on L - Carnitine? I do not know much at all about it. I know what it does, but I don ' t know if a suppliment helps. Thanks!
Good Luck! [ / icon_smile. gif]
firelady
Senior Member
Joined: 20 Aug 2003
Posts: 1506
Thu Feb 19, 2004 2: 14 pm    Post subject: Sorry
Carnitine ( LAC ) in any of it ' s forms does NOT help weight loss. I have explained before that all reputable studies with humans ( with or without needful oils ) have shown NO weight loss advantage. Only studies with one particular type of grotesque do show weight loss.
How can this be when in truth carnitine does help cells marshal fat? Well think a process where there are many steps that transpire in series. The wise can only go as fast as the slowest step ( imagine your car in traffic ). Unless LAC speeds the slowest step no incremental fat hang-up occurs. This type of course is what I interpret and research so you can believe or not. A diabetic might have a carnitine deficiency so if you are obese and a diabetic LAC might help with weight loss but at variance NO.
These supplements are inestimable, you do not need them for weight loss.
They do appear to have other good health effects ( for memory loss and some nervous disorders ) and have been shown not to be hazardous in the amounts normally taken.
An aside, there is much info on the WEB and much of it false ( case in point is that you can find as many anti - Atkins articles by reputable doctors as pro ). You need to look at primary sources.
beetledriver2
Senior Member
Joined: 27 Oct 2003
Posts: 414
Station: Illinois
Thu Feb 19, 2004 2: 32 pm    Post subject:
I found L - Carnitine in liquid form at www. vitaminworld. com. I bought two 16oz bottles of L - Carnitine for $16. 48. It was a buy one get one free deal. I read that the liquid form is better because it ' s easier to sink.
I know the tablets are fairly esteemed so I hope this helps anyone who ' s interested.
blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Spot: Durham, NC
Thu Feb 19, 2004 2: 52 pm    Post subject:
I have posted this before and will get the specialized journals if I can again as this is my area of research. There are studies ( not as rigorous as standard drug studies for the FDA ) that indicate for those people who suffer with insulin resistance ( which is not everyone ) that this help with weight loss. In addition this is something that Atkins himself routinely gave to his many patients and I know that I have seen benefits.
It is not the magic pill that will help everyone to lose weight. There is no such pill nor is there likely to ever be one based on current obesity research. However, it does benefit some people and I am living proof. This is a case of your appliance will vary. For some this will make all of the difference in the world ( those with PCOS, pre - diabetes, metabolic X syndrome, etc. ) because even Atkins is markedly slow for them. I present this for people to finish for themselves. There is research that indicates that it has some effect in specific patient populations and Dr. Atkins clearly gave it to his metabolically resistant patients. That ' s good enough for me.
Uncle Bitter
Senior Member
Joined: 23 Apr 2003
Posts: 290
Latitude: Georgia, USA
Thu Feb 19, 2004 2: 52 pm    Post subject: Snake Oil?
Snake Oil?
snake oil
noun
1. A worthless preparation fraudulently peddled as a cure for many ills.
2. Speech or writing intended to deceive; fake.
Bitter
[ / icon_wink. gif]
blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Station: Durham, NC
Thu Feb 19, 2004 2: 57 pm    Post subject:
Hey Bitter,
Since the low carb craze, this supplement has been hyped way to much, much like CLA. But it does have uses for some people. Marketing has messed up perceptions as with most things.
Not snake oil, but not the panacea either.
firelady
Senior Member
Joined: 20 Aug 2003
Posts: 1506
Thu Feb 19, 2004 3: 12 pm    Post subject: HI
Every single article from Medline ( peer reviewed studies ) shows NO incremental weight loss ( unless you ' re a particular kind of furry plug with whiskers ). From looking at the data it is possible that if you are obese with diabetes it MAY help. Weird IT WILL NOT. This is snake oil. The only way people can conclude for themselves is to look at peer reviewed PRIMARY sources. Anecdotal sources are the bread and butter of the pill saleman.
I ' m not putting down taking ALC for other purposes it can be a utile supplement especially if you have diabetes. Just in lineup to lose weight AND keep it off you need to change eating habits. Using pills probably will not work and will detract from learning new positive habits.
blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Locale: Durham, NC
Thu Feb 19, 2004 4: 29 pm    Post subject:
I won ' t consult with here because I don ' t thing it is well-timed and because I have work to do. I too do obesity research and am well brilliant with peer reviewed studies and journals. This supplement is no different than many others which also have none of the evidence you are demanding and yet we talk about them and people ask about them. In gospel, until the last few years there were not peer reviewed journal studies for the Atkins diet either, and yet it clearly worked.
kristov
Noted Member
Joined: 08 Dec 2003
Posts: 40
Thu Feb 19, 2004 5: 57 pm    Post subject: Ok....
Ok - so the deal is - in some people it has shown some effect - mainly those with diabetes / insulin resistance?
Safe to say: ( these two are questions )
1 ) it definately doesnt help everyone
2 ) it may help you but there is no real way to tell if it is scrap you
????
Chris
blueskyes2
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Joined: 11 Jun 2003
Posts: 2742
Seat: Durham, NC
Thu Feb 19, 2004 6: 16 pm    Post subject:
You somewhere have it right. I could tell it was segment only because without I lost nothing ( indeed nothing ) for over 6 months. This time around I have lost 42 pounds. I read everything about it from Dr. Atkins and other folks. The second time around on Atkins I knew I had insulin resistance problems because I had a trait that results from it. I followed exactly what Atkins outlined and I lost weight when I hadn ' t before. This is not 100 % proof as there are still some environmental factors that were different ( like age, for instance ), but it is pretty good evidence. It would not be publishable in a peer reviewed journal, however.
Bottom line,
If you have done the first two weeks of Induction properly ( no cheats, no lc foods, etc. ) then you can figure out if you are metabolically resistant by how much weight you lost ( see viand in DANDR ). Then you read Chapter 20 to determine if there are things you can do to help speed the loss along - one of which is L - carnitine.
If you ' re not metabolically resistant, then don ' t bother wasting your finances, just come from the plan and exercise.
firelady
Senior Member
Joined: 20 Aug 2003
Posts: 1506
Thu Feb 19, 2004 6: 50 pm    Post subject: hi
I hate to belabor this but misuse of mechanical info is one of my main bug - a - boos. On Atkins the lack was because the mainline establishment refused to check the correct experiment until recently. That is NOT the case for LAC it has been shown NOT to work by many peer reviewed studies eliminate maybe for those who are obese and diabetic. The only study in the literature that had any positive effect ( minor ) in humans had all the obese diabetic in the LAC group and all with little to lose in the other ( a miserably designed study ).
If you have diabetes you should consider taking LAC not for weight loss but because it has been shown to have a positive impact on some of the nerve impairment problems associated with diabetes. This is a big deal.
I ' m not trying to be mean. There is just no real evidence that LAC helps anyone with weight loss. This is not like the initial Atkins diet studies where people were trying to prove him wrong. Some of the people doing these studies initially believed in LAC. I am concerned with the pushing of this ( or any supplement that has not been proven ) both because of the amount and the focus to a nonuseful long term road. Everyone has stalls on any diet. The best way out of a stall is a jar ( Fat fast, other major change in food etc ) and then back to normal induction.
Lastly one major confusion that even some science students have a hard time with is that analogy DOES NOT Suggest Antecedent. If you get a positive result in an epidemiology type study it is a START not a beginning. Certainly we can not determine personally the effect of discrete elements of this diet at least not in the short term. I ' ve found that the woosh fairy comes pretty unpredictably. I ' m sure most of you find the same thing.
blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Bearings: Durham, NC
Thu Feb 19, 2004 7: 01 pm    Post subject:
OK, now I am being maligned and I don ' t appreciate it. I am not a science student and do actual salutary research. I am obese ( unfortunately ). I am pre - diabetic. That is my point exactly. I would suppose that there are others here who are as well. Let it drop. People can heap for themselves. I have a disposition to be unlatched minded and read all of the research - not just what is published in the journal that I personally publish in - before I make decisions.
Once again, The advice came from Dr. Atkins. If I am going to proceed from Atkins and believe his plan, why would I suddenly think that I know more than he did? If I did I wouldn ' t be fat.
L. T. Strife
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Joined: 02 Jan 2004
Posts: 374
Whereabouts: The heart of the Evil Empire
Thu Feb 19, 2004 10: 31 pm    Post subject:
I don ' t think we should dismiss anecdotal or testimonial information.
Science isn ' t everything. Maybe they haven ' t figured out yet who is affected. It ' s possible that in adjustment for it to help someone they need to have a certain physical makeup and that makeup hasn ' t yet been determined.
I don ' t think you can say it doesn ' t help anyone period ( based on my understanding of how much / how little it ' s been studied ), just that science has discovered it doesn ' t help everyone. There ' s a big difference.
Blueskyes believes it has helped her. It ' s possible that it has not. It ' s also possible that it has. Let her share her experience and don ' t discount it just because some study has reached a different conclusion.
Science is far from perfect. That ' s why we hear one study say eggs are bad for us and a study next week says they are good for us, then a study in three weeks tells us only the whites are good for us, etc. There are many paradoxical studies. I find personal testimonial information to often be easier to disect, try out, and understand.
Sari
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Joined: 19 Sep 2003
Posts: 1112
Locus: Australia!: )
Fri Feb 20, 2004 4: 50 pm    Post subject:
I have been looking for L - Carnitine here in Australia and am yet to find it... I am speaking to my doctor on Tuesday about possible medication I can take to help with my PCOS and insulin resistance... but not so sure with the amount of medications I have been taking lately... I am trying to stick to something natural..
The chemist coulnt help me.. but just gave me some dong quai and said that would help... do you guys know anything about dong quai and its effectiveness with insulin resistance?? the chemist just gave me a blank look when I mentioned insulin resistance and PCOS..
Sari [ / icon_smile. gif]
blueskyes2
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Joined: 11 Jun 2003
Posts: 2742
Spot: Durham, NC
Fri Feb 20, 2004 6: 22 pm    Post subject:
Hi Sari,
Hope you are feeling better.
Here is what I found on dong quai http: / / www. pour - tree. com / dongquai. htm
Apparently it is listed as the " female " ginseng. See quote below. It appears to have estrogenic properties. If what I understand from reading and from my Dr. is correct, many PCOS symptoms are actually helped with progesterone not estrogen. That is why he put me on BC with a higher level of progesterone. Some Drs. use straight progesterone pills or topical progesterone creams. Dong quai might well help some symptoms, thought, as there seems to be a variety of information on it.
People with insulin resistance ( pretty much any woman that has PCOS ) have a propensity to have lower levels of L - carnitine occuring naturally in their body. That ' s why Dr. Atkins had folks try it to help with their weight loss to see if they were one of those people. Because as an amino acid it is not absorbed markedly well, he had people take fairly large doses right from the start ( he said he started folks at 1500 mg - 500mg 3x a day ). So taking L - carnitine won ' t help with the PCOS, it may only help your body metabolize fat better which is the whole point of ketosis. You won ' t really know if it will work for you till you try it. Again it may help you if you are doing Atkins to lose weight, but won ' t help with PCOS. Since it is a fairly common amino acid, most vitamin stores like GNC, and Vitamin World carry it. I think Wal - Mart does now, too. You may be able to standardization it online, too. If you can ' t find it, you will still be OK since you are doing Atkins and a low carb diet is one of the best ways to help with PCOS.
Good luck, Sari. Hope you feel better ( hugs ).
" Dong quai has been called the " female ginseng " and is fine as an all end women ' s herb. It has been used for centuries in China for regulating the menstrual rotation and easing menstrual pain and cramping. It can be used to help women retrieve normal menstrual cycles after taking " the Pill. " It has proven helpful for relieving hot flashes during menopause. Dong quai can be used for insomnia and blood pressure stability for both men and women. ( The affect on blood pressure can be an overall lowering although sometimes it may rise slightly first, followed by a decline ). It can shorten PMS and may help anemia, suppressed menstrual flow, uterine hurting, abdominal pain after childbirth, dry belly, chronic pelvic disorders and constipation and headaches due to blood deficiency. Dong quai helps the liver utilize more oxygen and consequently can be applied in treating hepatitis and cirrhosis. It may also help with abnormal protein metabolism. Dong quai helps advance outmost blood vessels, increase circulation, and has been used as a mild senna.
Security: Not to be used during pregnancy. "
Sari
Senior Member
Joined: 19 Sep 2003
Posts: 1112
Stage: Australia!: )
Fri Feb 20, 2004 6: 36 pm    Post subject:
Hi Blueskyes..
Thank you so much for looking that up for me.. I use to take progesterone tablets but my doctor took me off them about a year ago.... With the information you posted I think Dong Quai might do the trick with a few of the symptoms.. I bewilderment if there is anything else that will help.. I will go and google it! heh [ / icon_smile. gif]
I will definately check out some online stores for the L - Carnitine.. it is worth a shot to see if it helps with the weight loss..
Thanks also for the well wishes... I am looking forward to the day I am healthy again!
Sari [ / icon_biggrin. gif]
Evrrdy
Senior Member
Joined: 08 Jun 2003
Posts: 1680
Where: US of A
Fri Feb 20, 2004 7: 11 pm    Post subject:
gggggrrrrrrrr
Hepatothermic therapy of obesity: thesis and an index of resources
M. F. McCarty
Pantox Laboratories, San Diego, California, USA
Manifest 17 August 2000; accepted 9 January 2001.; Available online 22 February 2002.
Abstract
Hepatothermic therapy ( HT ) of obesity is profound in the observation that the liver has substantial capacities for both fatty acid tinder and for thermogenesis. When hepatic fatty acid coals is optimized, the newly available free energy may be able to drive hepatic thermogenesis, such that respiratory quotient declines while basal metabolic rate increases, a circumstance evidently favorable for fat loss. Effective implementation of HT may miss activation of carnitine palmitoyl transferase - 1 ( rate - limiting for fatty acid beta - rapid oxidation ), an increase in mitochondrial oxaloacetate production ( required for optimal Krebs path activity ), and up - regulation of hepatic thermogenic pathways. The possible utility of various natural agents and drugs for achieving these objectives is discussed. Thinkable components of HT regimens encircle EPA - rich fish oil, sesamin, hydroxycitrate, pantethine, L - carnitine, pyruvate, aspartate, chromium, coenzyme Q10, green tea polyphenols, conjugated linoleic acids, DHEA derivatives, cilostazol, diazoxide, and fibrate drugs. Aerobic exercise training and very - low - fat, low - glycemic - index, high - protein or vegan food choices may help to install the hormonal environment good for to effective HT. High - dose biotin and / or metformin may help to prevent an excessive increase in hepatic glucose harvest. Since many of the agents contemplated as components of HT regimens are nutritional or food - derived compounds likely to be health possessory, HT is envisioned as an on - going lifestyle rather than as a interim Ôquick fixÕ. Initial clinical efforts to evaluate the likely of HT are now in progress.
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Propionyl - L - carnitine improves exercise performance and functional status in patients with claudication * 1, ACC Current Journal Review, Latitude 10, Issue 6, November - December 2001, Pages 32 - 33
W. R. Hiatt, J. G. Regensteiner and M. A. Creager
This one is a PDF so I can ' t paste it,, but there is a definite showing of improvement with the usage of PLC on exercise understanding.. at 3 months and further at 6 months. This may not * say * that it speeds weight loss, but we all know the benefits between weight loss and the aptitude to exercise.
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A new technique to raise night time advancement hormone release and a unrealized maturing hormone feedback control loop
T. B. Parr
Department of Medicine, University of Southern California, Los Angeles, USA
Celebrated 21 February 2000; accepted 1 June 2000.; Available online 22 February 2002.
Abstract
A new technique for controllable elevation of night time production hormone ( GH ) release in adult humans involves a synergy between verbal intake of the naturally occurring compounds acetyl - L - carnitine ( 500mg ) and L - ornithine ( 25–100mg ) taken at night time sleep after a 3 to 4 hour fast. The set point for normal hypothalamic GH release appears to incorporate a `whole body ' mitochondrial State 3 status `feed back loop ' controlled by systemic acetyl - L - carnitine levels.
Medical Hypotheses
Quarter 56, Issue 5, May 2001, Pages 610 - 613
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
Cardiomyopathy in minority, mitochondrial dysfunction, and the role of L - carnitine, American Heart Journal, Abode 139, Issue 2, Supplement 2, February 2000, Pages s63 - s69
Susan C. Winter and Neil R. M. Buist
The carnitine course
L - carnitine is a trimethylated amino acid derived from the diet and from endogenous sources. The main dietary sources of L - carnitine append red meats and dairy products, including human breast milk. Infants, with a low body protein mass, regularly depend on dietary sources for their carnitine supply, through adults are more capable of endogenous alliance. Consent depends on available endogenous protein sources with the conversion of trimethylated lysine derivatives liberated during muscle protein catabolism. The lysine derivatives differentiate enzymatic conversion to L - carnitine through an initial synthetic passage in the muscle and fathom a final conversion step in the liver.
Carnitine exists in a free form ( nonesterified ) or bound, as acylated ( esterified ) derivatives. Normally the distinguished acylcarnitine is acetylcarnitine from acetyl - CoA, but carnitine can also be esterified with many bound CoA derivatives, including the intermediates of - sparks and some amino acid intermediates. Carnitine is excreted mainly through the urine, although some is lost through bile. Ninety - five percent of the processed free carnitine is reabsorbed by the renal tubules, and the majority of the esterified carnitine is excreted in the urine, accordingly permitting excretion of the abnormal metabolites that accumulate in many inborn errors of fatty acid and amino acid metabolism. [33] Carnitine itself is not catabolized, and its only metabolic conversion involves the formation of such esters.
Esterification of carnitine is under the control of several enzymes, including carnitine palmitoyl transferase I ( CPT I ) on the outward ( cytosolic ) surface of the inner mitochondrial membrane and carnitine palmitoyl transferase II ( CPT II ) on the inner surface of the mitochondrial membrane. Fatty acyl CoA molecules are converted by CPT I to fatty acyl carnitines and touchy the membrane into the inner mitochondrial surface through a mitochondrial membrane carnitine acyl translocase. Once inside the mitochondria, CPT II re - esterifies the fatty acyl carnitine to generate a fatty acyl CoA and a free carnitine. The CPT I and CPT II enzymatic steps are reversible. Consequently the acyl groups can be jovial out of the mitochondria through reversal of the carnitine transport alley. [33 and 34]
Carnitine deficiency from a genetic defect in carnitine peace has not been described in any patients to date. The only primary defect in carnitine metabolism that has been identified is the absence of the muscle membrane carnitine transporter, which is inherited as an autosomal recessive defect. Inherited defects in activity of CPT I, CPT II, and carnitine membrane translocase have all been described. All these disorders of carnitine transport and transfer can decision in muscle dysfunction, including cardiomyopathy. [33 and 34]
In its role of transporter, L - carnitine modulates the availability of free CoA for mitochondrial metabolic processes. Because the inner mitochondrial membrane is impermeable to CoA, the availability of free CoA within the mitochondria requires the rapid removal of organic acids esterified to CoA. If the amount of available free CoA waterfall because of accumulation of acyl CoA derivatives for any reason, metabolic steps requiring free CoA can be compromised. This can conclusion in a rapid shutdown of mitochondrial energy crop and deterioration in heterogeneous cellular functions. Some of the steps affected by such a decrease in the free CoA / acyl CoA ratio inject conversion of pyruvate to acetyl CoA, - ketoglutarate to succinate, conversion of succinyl CoA to oxaloacetate, and - scorching. These disruptions of metabolism can event in lactic acidosis, hypoglycemia, and decreased ATP production. [33 and 34] Then, any genetic defect of mitochondrial metabolism and any metabolic or acquired defect resulting in carnitine deficiency can arrangement in a severe opinion to mitochondrial energy production, which may regard the heart.
In propionic aciduria, propionyl CoA accumulates within the mitochondria in massive quantities; free carnitine is then esterified, creating propionyl carnitine, which is then excreted in the urine. Because the supply of carnitine in the diet and from concord is limited, such patients eagerly generate carnitine deficiency as a fruition of the increased loss of acylcarnitine derivatives. This quality demands supplementation of free carnitine upper the normal dietary intake to continue to withdraw ( detoxify ) the accumulating organic acids. [35] A similar mechanism can befall with valproic acid, which is metabolized through CoA derivatives. [36]
Subordinate carnitine deficiencies
Carnitine deficiency can also be attributed to other causes. Dietary deficiency was identified in other wise normal infants fed infant soy formulas unsupplemented with L - carnitine. Subsequent identification of this problem, and supplementation of all infant formulas with adequate amounts of L - carnitine, has essentially eliminated this cause of inferior deficiency. However, deficiency is still being identified because of the use of total parenteral nutrition unsupplemented in L - carnitine. This deficiency is reported to happen more readily in children younger than age 2 years, maybe attributable to a decrease in muscle protein available for carnitine oneness, decreased carnitine singleness in the blooming child, or other yet to be described factors. [33, 37 and 38]
Other causes for junior carnitine deficiency may also be present. If the diet is adequate, impoverished pastime of carnitine can also payoff in a subordinate deficiency, which may eventuate with chronic malabsorption, such as cystic fibrosis, and chronic or acute diarrhea illnesses. Renal tubular dysfunction can conclusion in decreased reabsorption of L - carnitine and in total carnitine deficiency, as occurs in patients with the renal Fanconi syndrome. Loss of carnitine can also occur from either hemodialysis or peritoneal dialysis. [37]
* distinctive article that gives a ton of information,, while centered on inexperience cardiomyopathy, also takes the time to explain the processes and reactions of ACL.. plus, you might take the time to review the referrence list as it is extremely elaborate *..
_____________________________________________________________
I suppose I could go on all day with study after study.. however, the point is, the research is not always as black and white as being preposed. It can also be found in a myriad of places. Furthermore, to insinuate that one person ' s research is not as efficient than your own, is just down right insulting. Period.. We have a plethora of education levels, talents, strengths and weaknesses among us. Each of us is valid, and that should never be forgotten. Additionally, I don ' t know of a single case that started on humans, IN ANY FIELD!!! Shoot, the psych field would be seriously SOL if it were not for animal studies. There are research guidelines,, and when starting new research,, or even rehashing old tired research,, the use of animals is always a safe bet.. It ' s how we get our foot hold into human trials.. Animal research is not the end all of research, but rather the beginning,, and should NEVER be discounted. But, at the same time, it is not the end all of science either. Preliminary ( or pilot ) studies may be continuously done on rats,,, but until there is sufficient research on humans, nobody can conclude that it is only effective for rats.
Evrrdy
Senior Member
Joined: 08 Jun 2003
Posts: 1680
Location: US of A
Fri Feb 20, 2004 8: 17 pm    Post subject:
Ok ok,, I wasn ' t going to post any more of these, but this one, just has too much good and useful information for me not to share it..
Needless to say, it ' s a journal article, * long and abhorrant language usage * but it is great information none the less.. Anybody that wants to know more about how L - carnitine works can really benefit from reading it, as it takes you step by step through the processes.. * AND explains the effects of ketogenesis *
Early Human Development 53 Suppl. ( 1998 ) S43–S50
Review
Biological roles of L - carnitine in perinatal
metabolism
* ´ ´ Joaqu? n Arenas, Juan C. Rubio, Miguel A. Mart? n,
Yolanda Campos
´ ´ Centro de Investigacion Hospital Universitario 12 de Octubre, Avda de Andaluc? a, km 5. 4.,
28041 Madrid, Spain
Abstract
Carnitine performs a crucial role in the energy supply of tissues during fetal life and in the
neonatal period by controlling the influx of fatty acids into mitochondria. Carnitine also
facilitates the oxidation of pyruvate and branched chain amino acids, and contributes to the
protection of cells from the deleterious actions of acyl CoAs. Carnitine further acts as a
secondary antioxidant, favouring fatty acid replacement within previously oxidatively damaged
membrane phospholipids. Availability of L - carnitine is essential in the developing fetus for
processes underlying fetal maturation. L - carnitine is also essential for development of hepatic
ketone synthesis, a central pathway for neonatal energy metabolism. Ketone bodies inhibit the
oxidation of both glucose and lactate, sparing these metabolic substrates for biosynthetic
functions. Ó 1998 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: L - carnitine; Beta oxidation; Fetal maturation; Energy metabolism; Perinatal
metabolism; Antioxidant
1. Carnitine metabolism
About 75 % of the carnitine source for the body stores comes from the diet: red
meat in adults and human milk in infants are the main sources. In man the liver and
the kidney synthesize the remaining 25 % from the immediate precursor gamma
butyrobetaine: protein - bound lysine and methionine are required for carnitine
biosynthesis [12]. Carnitine is present in tissues and biological fluids in free and
esterified forms. In humans, acylcarnitine esters account for some 25 % of total
* Corresponding author. Tel.: 134 - 1 - 3908598; fax: 134 - 1 - 3908358; e - mail: jarenas@h12o. es
0378 - 3782 / 98 / $ – see front matter Ó 1998 Elsevier Science Ireland Ltd. All rights reserved.
PII: S0378 - 3782 ( 98 ) 00064 - 4
S44 J. Arenas et al. / Early Human Development 53 Suppl. ( 1998 ) S 43–S 50
carnitine in serum and for about 15 % of total carnitine in liver and skeletal muscle
[8, 9, 12]. Total carnitine concentration in human tissues is higher in the heart and
skeletal muscle than in the liver and the brain. These values reflect the higher rates of
fatty acid oxidative metabolism in the former tissues [12]. Because of the bulk of
skeletal muscle and its great carnitine concentration, most of the total body carnitine
is stored in muscle [8, 12]. The remaining body carnitine is in the heart, liver and
kidney, with less than 1 % in biological fluids. Carnitine in blood is much less
concentrated than in tissues [12].
Consequently carnitine, either introduced in the diet or synthesized de novo in the
liver and kidney, must be actively concentrated from the blood into fatty acidmetabolizing
organs, such as skeletal muscle [12]. Cell receptors with high affinity
for carnitine have been identified in muscle and heart cells, and cultured fibroblasts
[12]. The liver and the brain have low - affinity receptors for carnitine, while the
intestinal epithelial cells and the renal tubular cells have intermediate - affinity
receptors for carnitine [12]. The kidney, besides its contribution carnitine biosynthesis,
is crucial in regulating the plasma and tissue levels of carnitine. The renal
threshold for free carnitine is similar to the concentration of carnitine in plasma, and
the proximal tubule actively transports carnitine across its membrane, thus minimizing
the loss of carnitine from the body [3].
Therefore, a complex metabolic equilibrium exists between the various carnitine
fractions in the different body compartments, and between the carnitine pool of
tissues and blood, as well as the fraction excreted in the urine.
2. Old and new biological roles of L - carnitine
An overview of the main physiological roles of L - carnitine is shown in Table 1.
Carnitine is a quaternary amine, synthesized from the amino acid lysine, which
performs a crucial role in energy supply by controlling the influx of long - chain fatty
acids into mitochondria. L - carnitine, two carnitine palmitoyl transferases, CPT I and
II, located respectively in the outer and inner mitochondrial membrane, and a
carnitine - acylcarnitine translocase embedded in the inner mitochondrial membrane,
are required in mammalian tissues to transfer long - chain acyl CoAs across the inner
Table 1
Physiological roles of L - carnitine
1 Mitochondrial long - chain fatty acid oxidation
2 Activation of aerobic glycolisis: Stimulation of pyruvate dehydrogenase complex
3 Enhancement of respiratory chain function
4 Buffering of the mitochondrial acyl CoA / CoA couple
5 Scavenger system for acyl groups
6 Peroxisomal fatty acid oxidation, intracellular communication
7 Branched - chain amino acid metabolism
8 Membrane stabilization
9 Donor of acetyl groups for biosynthesis ( e. g. acetyl choline )
10 Antioxidant network
J. Arenas et al. / Early Human Development 53 Suppl. ( 1998 ) S 43–S 50 S45
membrane for beta oxidation in the matrix [7]. Furthermore, intramitochondrial
carnitine and the matrix enzyme carnitine acetyltransferase ( CAT ) can react with
short - and medium - chain acyl CoAs to produce acylcarnitines, which can be shuttled
out of mitochondria [7, 12, 26]. Through this mechanism, carnitine is able to modulate
the intracellular concentrations of free CoA and acetyl CoA via the reversible
formation of acetylcarnitine. Therefore, besides shuttling long - chain fatty acids into
mitochondria, carnitine facilitates the oxidation of branched - chain ketoacids, and by
preventing their accumulation it contributes to the protection of cells from the
potentially membrane - destabilizing acylCoAs [26]. Carnitine may also shuttle acyl
moieties, shortened by the peroxisomal beta oxidation system, from peroxisomes to
mitochondria for further oxidation [12].
The relevance of carnitine in intermediary metabolism is supported by its role in
the control of ketogenesis. Malonyl CoA, the first intermediate of fatty acid
biosynthesis, is a potent inhibitor of CPT I, the acyltransferase located in the outer
membrane in mitochondria, therefore suggesting a reciprocal control of hepatic fatty
acid biosynthesis and oxidation by malonyl CoA and carnitine in normal and ketotic
states [4]. With a carbohydrate diet, when the plasma ratio of glucagon to insulin is
low, the malonyl CoA concentration rises with concomitantly enhanced fatty acid
synthesis and suppression of fatty acid oxidation [13]. Conversely, in the fasting state
or uncontrolled diabetes, where the plasma glucagon to insulin ratio is high, the
malonyl CoA levels fall and carnitine levels increase in the liver. Fatty acid synthesis
is then diminished and CPT becomes depressed, favouring fatty acid oxidation and
ketogenesis [13].
In two recent reports, we have demonstrated that carnitine plays a pivotal role in
the final steps of carbohydrate metabolism as well as in the regulation of the
mitochondrial respiratory chain [2, 3]. Carnitine facilitates the oxidation of pyruvate
via pyruvate dehydrogenase complex ( PDH ) stimulation [2]. Moreover, carnitine
induces an increase of the respiratory chain enzyme activities in muscle, probably by
mechanisms involving mitochondrial DNA [19].
An emerging and fascinating role of L - carnitine is related to its capacity as an
antioxidant. Carnitine and carnitine palmitoyl transferase can be considered integral
components of the membrane phospholipid fatty acid turnover in human cells [1]
( Fig. 1 ). Since this pathway is essentially related to the secondary antioxidant
response to oxidatively damaged membrane phospholipids, it may be considered that
carnitine takes part in the antioxidant network as a member of the secondary defence
line. Moreover, we have documented an alteration in the acyl - flux regulated by CPT
and carnitine in membrane erythrocytes from uremic patients [11]. In the latter, there
is a marked increase in free radical formation, and therefore in cell membrane
peroxidation. This process must be followed by proper membrane phospholipid
repair, in which carnitine exerts a pivotal role. We found that L - carnitine supplementation
improved membrane phospholipid fatty acid turnover, thus supporting the
role of carnitine as a part of the secondary antioxidant system.
Furthermore, carnitine, via acetylcarnitine formation by CAT, represents a physiological
means of providing acetyl groups for biosynthesis of some compounds [26].
This is particularly relevant in the formation of the neurotransmitter acetylcoline in
S46 J. Arenas et al. / Early Human Development 53 Suppl. ( 1998 ) S 43–S 50
Fig. 1. The carnitine system and membrane phospholipid repair process. PLP: phospholipids; PLP - OOH:
phospholipid hydroperoxide; Cn: carnitine; acyl Cn: acyl carnitine; CPT: carnitine palmitoyl transferase;
LAT: lysophospholipid acyl CoA transferase; ACS: acyl CoA synthetase.
neurons [30]. Acetylcarnitine exerts, therefore, a cholinomimetic activity, and through
this function may be critical for normal brain development in mammals.
3. Carnitine in perinatal metabolism
In fetal tissues of mammals, metabolic energy is obtained mainly from the
oxidative metabolism of carbohydrates. Birth represents a sudden increase in energy
requirements. In addition to ongoing needs for growth and differentiation, there are
new requirements to generate metabolic energy for breathing, movement and
maintenance of body temperature [24]. After delivery, the normal neonate adapts to
fatty acids as a major source of calories. Within hours, accelerated lipolysis elevates
free fatty acid concentrations and fatty acids are supplied by a high fat diet of milk
[24].
The mammalian carnitine pool is heavily dependent on exogenous intake. The
transplacental transport of carnitine or precursors from the maternal plasma appears
important for the formation of carnitine stores in fetal tissues [6, 27]. In term placenta,
the maximal carnitine transfer is far in excess of the estimated carnitine requirements
[24]. However, it is unknown whether carnitine biosynthesis in the fetus is a
significant contributor to its carnitine status. It seems that transplacental transport may
ensure sufficient amounts of carnitine even in the absence of carnitine biosynthesis in
fetal tissues [24]. Carnitine is stored in fetal tissue in increasing amounts during the
last part of gestation, and tissue carnitine stores at birth are directly related to
gestational age [23].
Availability of L - carnitine is essential in the developing fetus, where L - carnitine is
J. Arenas et al. / Early Human Development 53 Suppl. ( 1998 ) S 43–S 50 S47
essential for processes underlying fetal maturation. Given that in fetal tissues of
mammals the metabolic energy is obtained mainly from the oxidative metabolism of
carbohydrates, the strong dependence on L - carnitine is apparently puzzling. As stated
above, carnitine regulates the activity of PDH, an enzyme that plays a central role in
the final steps of aerobic catabolism of glucose [2]. Moreover, carnitine is a potent
stimulator of the activities of the mitochondrial respiratory chain [19]. In fulfilling
these two biological roles, carnitine provides the energy supply necessary to meet the
energetic demands of fetal tissues. This fact could be particularly relevant in the
developing brain, where beta - oxidation accounts for 25 % of energy production [14],
the remainder being dependent upon the oxidative metabolism of glucose.
Pulmonary surfactant production is an important process in fetal maturation.
Carnitine has been shown to be more effective in inducing pulmonary surfactant
production and lung maturation in both rats and humans than betamethasone, a drug
commonly administered to women in preterm labor to induce fetal lung maturation
[21]. The mechanisms whereby L - carnitine acts as an inductor of pulmonary
surfactant production are unknown. It is widely accepted that membrane phospholipid
fatty acid turnover is related to the production of pulmonary surfactant production.
Since carnitine is an integral component of the membrane phospholipid fatty acid
turnover in human cells [11], it is possible that carnitine causes lung maturation via
membrane phospholipid repair activity.
After delivery, the neonate is faced with marked metabolic challenges. Many vital
functions are assumed by the mother during prenatal life. With the interruption of the
continuous supply of placentally transported nutrients, the neonate depends on the
utilization of metabolic fuels derived from endogenous sources [15].
The release of energy - yielding substrates from stores accumulated prenatally is
initiated by hormonal changes at birth. Glycogen from muscle, liver and other tissues
represents a minor source of metabolic fuel for the newborn. Glycogen stores are
exhausted within hours after birth. Although fat constitutes some 15 % of the body
weight, the proportion may vary in newborn infants after altered gestation [24].
The rapid increase in free glycerol and free fatty acids ( FFA ) in plasma of newborn
infants give the first evidence of an accelerated release of these substrates from
adipose tissue. However, the interpretation of plasma concentration is complicated; it
may be high because of increased release or decreased uptake by tissues [24].
Adipose tissue has been shown to be influenced by the adaptive mechanisms
necessary for the neonate to cope with the extrauterine environment. L - carnitine is
high in brown fat, which is important in thermogenesis [16], and is high in all body
tissues of cold acclimatized animals [28], suggesting a role in adaptation to the
extrauterine environment.
Beta oxidation of FFA becomes increasingly important for energy production in
adipocyte cells after birth [15]. The accumulation of FFA occurs when the glycogen
stores become depleted. The increase in carnitine - dependent fatty acid oxidation is
related to energy requirements. The availability of carnitine may affect the regulatory
processes by which adipose tissue provides metabolic fuels for other tissues [24].
Liver glycogen stores accumulate during late fetal life in all mammals, but are
rapidly mobilized at birth to provide glucose for tissues and cells that are entirely
S48 J. Arenas et al. / Early Human Development 53 Suppl. ( 1998 ) S 43–S 50
dependent on glucose to maintain their function. The supply of FFA to the liver
depends on the amount of adipose tissue stores and fatty acid release. Several
regulatory mechanisms operate for the control of hepatic fatty acid oxidation [18].
Just after birth, there is a transient hypoglycemia, an increase in plasma glucagon and
catecholamines, and a fall in plasma insulin. The production of ketone bodies in the
liver is accompanied by an increase in carnitine content and seems to be regulated by
CPT - 1. This enzyme controls the rate of activated FFA into mitochondria [18]. The
increase in the capacity for FFA oxidation and ketogenesis comes from a decrease in
lipogenesis and malonyl CoA concentration. This mechanism may ensure a sensitive
response to decreased availability of carbohydrates and provide control of ketone
body production as alternative fuels in the fasting status [15, 18].
At birth, the fetoplacental transfer of carnitine is interrupted. Before the onset of
feeding the neonate heavily depends on fetal carnitine stores and on endogenous
carnitine biosynthesis. Early postnatal ketogenesis is stimulated by carnitine from
milk [15, 24]. Fatty acid oxidation in the liver provides cofactors ( e. g. Acetyl CoA,
NADH and ATP ) for gluconeogenesis and ketogenesis [4]. Early neonatal hypoglycemia
may derive in part from reduced gluconeogenesis and may relate to a lower
capacity to oxidize FFA. After birth there is a period in which FFA accumulate in
tissues to a point where oversaturation of mitochondrial beta - oxidation is provoked.
Then, FFA may be increasingly metabolized in peroxisomes where their chainlengths
are shortened. These shortened fatty acids are converted to acylcarnitines and
may be transferred into mitochondria for further oxidation [4].
Systemic carnitine deficiency develops when cellular uptake and renal excretion of
carnitine is not balanced by endogenous synthesis and exogenous intake [12].
Endogenous synthesis of carnitine is limited in the neonate by low levels of gamma
butyrobetaine hydroxilase, the enzyme which catalyzes the final step of the carnitine
synthetic pathway. Critical co - factors for the carnitine biosynthetic pathway include
S - adenosylmetionine, pyridoxal phosphate, iron, ascorbic acid, nicotinic acid and
alpha - ketoglutarate. Deficiency of any of these compounds impairs carnitine biosynthesis
[17].
Premature infants, who are born with the lowest stores of carnitine, cannot achieve
adequate carnitine homeostasis without an exogenous supply [25]. Therefore,
premature infants receiving unsupplemented infant formula, breast milk or parenteral
hyperalimentation are at high risk of developing systemic carnitine deficiency [6, 29].
Infants receiving total parenteral nutrition have been shown to exhibit biochemical
signs of impaired fatty acid metabolism [5, 10]. Poor carnitine availability in
premature infants may hamper adequate extrauterine growth despite apparently
adequate caloric intake through inefficient use of available substrates for energy
production [22].
In a recent report [20] Iafolla and Roe suggested that premature infants suffer from
systemic carnitine deficiency, which is clinically significant, and is correctable by
supplementation. In addition, they reported that premature infants are intrinsically
deficient, in that they are unable to adequately synthesize enough carnitine to meet
their metabolic demands, and that apnea, hypotonia, poor weight gain, delayed
development, and gastrointestinal reflux in very low gestation premature infants are
clinical manifestations of an untreated systemic carnitine deficiency [20].
J. Arenas et al. / Early Human Development 53 Suppl. ( 1998 ) S 43–S 50 S49
Acknowledgements
This study was supported by grants from FIS 98 / 1413, Ministry of Health, Spain,
and from Sigma Tau. J. C. Rubio was supported by ISC grant 97 / 4260, and M. A.
´ Mart? n by a grant from FIS.
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blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Location: Durham, NC
Fri Feb 20, 2004 9: 01 pm    Post subject:
Thanks for all of the journal articles, Evrrdy. What I found particularly interesting was the following.
" In a recent report [20] Iafolla and Roe suggested that premature infants suffer from systemic carnitine deficiency, which is clinically significant, and is correctable by supplementation. "
Guess who was a premie? [ / icon_eek. gif] Well, that might explain why I have a deficiency and then why supplementation works for me. Who knows? One thing I noticed is that when I take L - carnitine my ketostix registered far greater levels of ketosis than I ever was able to achieve when I did Atkins before without the carnitine. My belief is that it is helping me to get into a level of ketogenesis that " normal " people enjoy.
Very informative. Thanks a bunch! [ / icon_biggrin. gif]
underdog
New Member
Joined: 21 Jan 2004
Posts: 19
Fri Feb 20, 2004 9: 12 pm    Post subject:
I HAD STOP LOSING WEIGHT UNTIL I STARTED TAKING L - CARNITINE [ / icon_cool. gif].
I HAVE LOST 5LBS IN TWO WEEKS TAKING L - CARNITINE ALONG WITH FISH OIL.
firelady
Senior Member
Joined: 20 Aug 2003
Posts: 1506
Fri Feb 20, 2004 9: 29 pm    Post subject: HI AGAIN
SO U CAN SHOOT ME NOW BUT NONE OF THE ARTICLES ABOVE SHOW WEIGHT LOSS. LAC HAS SOME VERY GOOD EFFECTS AND PLAYS AN IMPORTANT ROLE IN THE BODY. THERE ARE HUNDREDS OF ARTICLES ON ITS EFFECTS LISTED ON MEDLINE ( ONE OF THE PREMIER MEDICAL SEARCH ENGINES ) WHICH ANYBODY HERE CAN ACCESS AT THEIR LOCAL LIBRARY. AS I SAID BEFORE IT DOES PLAY A ROLE IN METABOLISM THAT WOULD ONLY RESULT IN WEIGHT LOSS IF THAT WAS THE RATE LIMITING STEP IN YOUR WEIGHT LOSS.
I SUPPOSE IT IS HOPELESS TO EXPLAIN CAUSE AND EFFECT BUT IT IS IMPORTANT. WEIGHT LOSS ON THIS ( OR ANY DIET ) CAN BE ERRATIC. cLAIMING A POSITIVE EFFECT FOR A SINGLE CHANGE IS SIMPLY NOT POSSIBLE WITH A ONE PERSON SAMPLE ESPECIALLY FOR A SHORT TERM EFFECT THERE ARE JUST TOO MANY VARIABLES.
" THERE ARE THINGS NOT EXPLAINED BY SCIENCE. " WELL I AGREE GOD WORKS MIRICLES BUT I DON ' T BELIEVE IN DIVINE INTERVENTION ON THINGS LIKE THIS. ALSO I AGREE THERE ' S SO MUCH WE DO NOT UNDERSTAND ALL THE MORE REASON NOT TO JUMP TO CONCLUSIONS. yOU HAVE MONEY TO BURN THERE ARE MANY SUPPLEMENTS OUT THERE TO BUY THAT ARE ESSENTIAL TO YOUR BODY THAT YOU COULD BE DEFICIENT IN. HOW MANY PILLS DO YOU WANT TO TAKE PER DAY AND HOW MUCH MONEY DO YOU WANT TO SPEND?
p. s. tHERE ARE SEVERAL ARTICLES ON hgh AND lac IF THERE EVER IS
A CONNECTION TO TRIMMING YOUR BODY THIS MAY BE IT.
Evrrdy
Senior Member
Joined: 08 Jun 2003
Posts: 1680
Location: US of A
Fri Feb 20, 2004 10: 06 pm    Post subject:
This is becoming exhausting. Please don ' t shout, there is never a reason to shout. The articles that were provided have many purposes. The main one is for everyone to be informed. The picture you paint is a very glim one indeed, and as you have continually touted your sources, you have also not convinced me that they are the complete picture. The one thing I will agree with you on is that there are many supplements that claim results and we shouldn ' t go hog wild with spending our hard earned dollars on them. However, there are many benefits to taking carnitine. No, they are not for everyone,, and as informed consumers it is our job to determine what is right for each of us. For me,, I would gladly ditch every supplement in the world,, in exchange for essential oils ( 3 / 6 / 9 ) and l - carnitine... FOR ME.. it works.. why??? I have no idea.. but for me.. it does. It is completely and totally unfair of you to come in claiming that you have all the answers and everybody else is wrong. Again,, I will repeat, that we are all valid. Not a single one of us,, ( or any research ) has all the answers. To even insinuate such puts you at a much exalted level above all human capacity...
I ' m trying to be nice about this.. continue to scream at me.. and this will turn ugly. case closed.
northernlady
Senior Member
Joined: 23 Apr 2003
Posts: 3458
Location: Middle of the country! Columbia MO
Sat Feb 21, 2004 12: 37 am    Post subject:
You know, I really wish ONE of you was right. That way this whole discussion could be put to rest and the antagonism would stop. But the reality is that all the world ' s scientists and doctors have limited amount of knowledge about weight loss, and most of us ( yes even those of you that * study * weight loss have even less. Communicating that limited information, while taking into account every nuance and variable we know of, and trying to discount the nuances and variables we don ' t know about - is an even MORE daunting task. I really think all the going back and forth and postings has to end because nothing but hurt feelings is being accomplished here. Please consider who you are all talking to - - we are your friends and we all care about all of you.
We, all of us here on this board, are struggling with trying to figure out why some people overeat - and never gain weight - - - - all the way to people who look at food, breath in the smell and gain weight ( the is some anecdotal information on the aroma causing weight gain [ / icon_eek. gif] ) Why can I run 4 days a week, lift weights, walk everywhere - burn a supposed 1600 calories a day - - eat 1500 calories a day and I am still only 25 - 30 lbs down from my starting weight.
I ' m sure these suppliments worked on some level at some point for someone - - I am also sure someone somewhere is making lots of money on exaggerated claims and funding studies to prove it does work. So, quite frankly, I don ' t cares who is right. I do care however for the integrity of this board - which is first and foremost a Support Board, not a sales pitch or a scientific peer review committee.
jennicolleen
New Member
Joined: 18 Feb 2004
Posts: 2
Location: Milan, MI
Sat Feb 21, 2004 4: 56 pm    Post subject:
This has been quite the interesting topic. [ / icon_smile. gif]
I just bought a bottle of L - Carnitine. Does anyone know at what dose I should begin taking it? I ' m also noticing that people are taking it with fish oil? Is this what I should do too? I currently take Atkins Essential Oils, Multivitamin, Atkins Accel, and Magnesium, Calcium & Zinc.
If anyone could help I ' d appreciate it.... Or perhaps there is a source I could check?
Thanks!
Jennifer [ / icon_razz. gif]
L. T. Strife
Senior Member
Joined: 02 Jan 2004
Posts: 374
Location: The heart of the Evil Empire
Sat Feb 21, 2004 9: 06 pm    Post subject:
Also, our brains are funny things. Even if it ' s just acting as an expensive plecebo who is it really hurting?
I agree that we should be careful not to insinutate that it ' s the magic pill. I think everyone on this thread would agree it ' s not.
But it ' s possible that it does help weight loss and that information should be shared. As more people try it they can share their experiences and maybe we ' ll begin to see a pattern of who it helps and who it doesn ' t.
With regards to cause and effect: Weight loss is difficult. I personally have to try many things and see what works. Even then I ' m not sure exactly what is affecting my weightloss and what is just superstition. But I want people to tell me what they think is working for them. Just like I want to tell people what I think works for me. Then I can keep trying things and possibly see improvements.
I see a lot of posts that say things like " I drink soda and it doesn ' t affect me at all. " Well that ' s a nice opinion but really they don ' t KNOW that it ' s not affecting them. Because maybe if they weren ' t drinking the soda they would lose faster. Because since they can ' t drink it and not drink it at the same time there ' s no real way to KNOW if their statement is true.
However, that doesn ' t make their statement invalid either. If I hear enough people say that they don ' t think drinking soda is affecting their weightloss then I might conclude that in general, for many people, drinking soda has such an insignificant affect that I can drink it and still maintain a level of weightloss I ' m satisfied with.
So even though their opinions are based on their perceptions and not on fact, I can still gain valuable information that will help me shape my weight loss program.
I think hearing what people think works and what they think doesn ' t work has a lot of value, regardless of its scientific precision.
So please keep sharing your opinions folks. They do help.
blueskyes2
Senior Member
Joined: 11 Jun 2003
Posts: 2742
Location: Durham, NC
Sun Feb 22, 2004 4: 52 am    Post subject:
Hi Jennifer,
If you are already taking Essential Oils then you are getting many if not most of fish oils that you need so you probably don ' t need anything else. A lot of people take 1000 mg a day, 500 in the morning and 500 in the evening. Personally I started with 1500 mg based on recommendations that Dr. Atkins made in his book. If you have the book, you can find out more about the supplement there.
Northernlady, I apologize for bringing this topic up as it caused so much upset. There were several reasons I did. One, because this is something that Dr. Atkins explicitly mentions in his book and two because other sites I have been to are curious and discuss it. I was sharing the information much as I would share that Dannon has a new yogurt, etc. I tried to share a quote that was not heresay but was more informational. I am not hawking it and I am sorry if it appeared I was. I value everyone ' s experience and like to hear pros and cons of everything so that I can make my own decision. That was my intention. If we can ' t express our experiences here, anectdotal or not, then why are we here?
I won ' t mention this supplement again since it causes such discord. I just feel bad about the need for censorship because we can ' t seem to respect each other.
bluehex
Senior Member
Joined: 03 Dec 2003
Posts: 2663
Location: Warsaw, Poland
Sun Feb 22, 2004 7: 07 am    Post subject:
Blueskyes, thank you for bringing this topic up. I greatly appreciate the information - I ' ve been looking for this info anyway, because I ' m in a stall ( 5 months now ) and really am out of choices. I thought of taking L - Carnitine, before I saw it, now I ' ve made a decision.
Now, I know it is not guaranteed and that reserarch results are fuzzy. But it MIGHT help. And that ' s all I need at the moment. As L. T. Strife said, even if it ' s just an expensive placebo, who cares? Expensive? Sure. But it ' s MY wallet, firelady, and I don ' t need a guardian for it, thank you.
From all that has been stated in this topic, I know now for sure it is not going to harm me, and it is just possible it might help. Now it is up to me to try it or not.
Blueskyes, I didn ' t take your info as advertising carnitine or even recommending it - you just presented it as a possibility, for everyone ' s consideration, just as you did with BMR and other things. We are all adults here ( well, most of us ), capable of making our own decisions. Please, keep the information comming, because your contributions are always valuable and interesting.
northernlady
Senior Member
Joined: 23 Apr 2003
Posts: 3458
Location: Middle of the country! Columbia MO
Sun Feb 22, 2004 4: 20 pm    Post subject:
Blueskyes - - - I agree totally with Bluehex - - Your post was not advertizing or trying to sell a product. All I was doing was to stress that this board is for support, sharing of information - both personal experience and those of an " FYI " nature ( which is how most of us read your initial post ), and daily encouragement for those of us who are struggling with weight concerns.
I think it is hard for us communicating in this venue to really understand what each other is saying - - so I see this not as a problem among " friends ", but rather as a problem with the crude ( yes - even though we have evolved to an instantaneous cyber community, we really don ' t get the " full " communciation, because we can ' t see, smell, touch, hear each other ) form of communication to relay critical, detailed and specific information.
I respect those among us who are the scientists. In more times than I can count, you all have saved me and others from " reading " something and not really " understanding " it. You have pointed out what might be a scam, what might be incorrect interpretations, or what might be another way of looking at the ' science ' behind low carbing. I offer no expertize in those areas and I look to all of you for help decifering what I need to know. For that, I respect all of you and hope we can get past this particular thread and move on.
Thanks to all of you for an interesting and thought provoking thread - both for the information and for the opportunity to evaluate how we " talk " to one another.
yaz180
Established Member
Joined: 07 May 2007
Posts: 142
Thu Feb 21, 2008 9: 33 pm    Post subject:
so bluehex, did the l carnitine work for you that time 4 years ago?
bluehex
Senior Member
Joined: 03 Dec 2003
Posts: 2663
Location: Warsaw, Poland
Thu Feb 21, 2008 11: 03 pm    Post subject:
I had to stop taking it before it could produce any results - it caused me some really strong stomach aches. So I still don ' t know if it works... [ / icon_confused. gif]
Manu
New Member
Joined: 28 Feb 2008
Posts: 2
Location: France
Thu Feb 28, 2008 8: 40 pm    Post subject:
Please ignore my last message, it worked! I can ' t post in all threads, which annoys me sometimes.
Anyway, L - Carnitine makes me jittery, like coffee. I take that to mean its working.