Get More Vitamin D

Biochemist proposes worldwide policy change to step up daily vitamin D intake

Vitamin D is effective in reducing frequency of many diseases and cost of medical care, stresses UC Riverside’s Anthony Norman

Anthony Norman, a leading international expert in vitamin D, proposes worldwide policy changes regarding people’s vitamin D daily intake amount in order to maximize the vitamin’s contribution to reducing the frequency of many diseases, including childhood rickets, adult osteomalacia, cancer, autoimmune type-1 diabetes, hypertension, cardiovascular disease, obesity and muscle weakness.

“A reduction in the frequency of these diseases would increase the quality and longevity of life and significantly reduce the cost of medical care worldwide,” said Norman, a distinguished professor emeritus of biochemistry and biomedical sciences at the University of California, Riverside. “It is high time that worldwide vitamin D nutritional policy, now at a crossroads, reflects current scientific knowledge about the vitamin’s many benefits and develops a sound vision for the future.”

Currently, the recommended daily intake of vitamin D in the United States is 200 international units (IU) for people up to 50 years old; 400 IU for people 51 to 70 years old; and 600 IU for people over 70 years old. Today there is a wide consensus among scientists that the relative daily intake of vitamin D should be increased to 2,000 to 4,000 IU for most adults.

“Worldwide public health is best served by a recommendation of higher daily intakes of vitamin D,” Norman said. “Currently, more than half the world’s population gets insufficient amounts of this vitamin. At present about half of elderly North Americans and Western Europeans and probably also of the rest of the world are not receiving enough vitamin D to maintain healthy bone.”

Reporting in a review paper in the July 28, 2010, issue of Experimental Biology and Medicine, Norman and Roger Bouillon of the Laboratory of Experimental Medicine and Endocrinology at the Katholieke Universiteit Leuven, Belgium, warn that if the current nutritional guidelines for vitamin D remain unchanged, rickets and osteomalacia, which could be easily prevented, will continue to occur.

They add that if the present guidelines for vitamin D intake are strictly implemented and applied worldwide to pregnant or lactating women, newborns and children, the occurrence of rickets in infants could be effectively eradicated.

Norman, the first author of the review paper, and Bouillon note that if the daily dietary intake of vitamin D is increased by 600-1000 IU in all adults above their present supply, it would bring beneficial effects on bone health in the elderly and on all major human diseases (e.g., cancer, cardiovascular, metabolic and immune diseases).

The researchers add, however, that if the vitamin D dietary intake were increased to 2000 IU per day and even more for subgroups of the world population with the poorest vitamin D status, it could favorably impact multiple sclerosis, type-1 diabetes, tuberculosis, metabolic syndrome, cardiovascular risk factors and most cancers.

About vitamin D:

Also known as the “sunshine vitamin,” vitamin D was discovered 90 years ago as a dietary agent that prevented the bone disease rickets.

Exposure to the sun is the body’s natural way of producing the vitamin. Skin exposed to solar UVB radiation can produce significant quantities of vitamin D. But this vitamin D synthesis is reliably available year-round only at latitudes between 40 degrees north and 40 degrees south. A combination of sunshine, food, supplements, and possibly even limited tanning exposure can raise the daily intake of the vitamin to 2000 IU.

Vitamin D is itself biologically inert. Its biological effects result only after it is metabolized first in the liver and then in the kidney – a process that converts the vitamin into a steroid hormone.

The best sources of unfortified foods naturally containing vitamin D are animal products and fatty fish and liver extracts like salmon or sardines and cod liver oil. Vitamin D-fortified food sources in the United States (the fortification levels aim at about 400 IU per day) include milk and milk products, orange juice, breakfast cereals and bars, grain products, pastas, infant formulas and margarines.

Vitamin D excess can cause health problems such as hypercalcemia, vomiting, thirst and tissue damage. The precise upper limit for daily vitamin D intake is not well defined.

Vitamin C in the blood stream is directly related to fat oxidation

Low amounts of vitamin C correlates with increased body fat and waist measurements. Nutrition researchers at Arizona State University report that the amount of vitamin C in the blood is directly related to fat oxidation during both exercise and at rest.

The study shows that those who consume adequate quantities of vitamin C oxidize 30% more fat while doing normal exercises than individuals with an inadequate quantity of Vitamin C consumption.

The research however, does not imply that vitamin C can be considered the new remedy for obesity and the new means of causing weight loss. Rather, it establishes that consuming insufficient quantities of vitamin C is liable to hamper any efforts of weight loss. Continue reading “Vitamin C in the blood stream is directly related to fat oxidation”

Good Fat, Bad Fat: The Facts About Omega-3

I found an interesting article on WebMD today about Fish Oil and Omega-3. I’ve been a long time reader of Mens Health Magazine and they’ve touted the merits of fish oil for a long time.

Check out the following and let me know what you think.

Think all dietary fat is the same? Guess again
By Colette Bouchez
WebMD Weight Loss Clinic-Feature

If you ask folks what food group they should avoid, most will probably answer “fats.” While it’s true that, in large amounts, some types of fat are bad for your health (not to mention your waistline), there are some we simply can’t live without.

Among them are the omega-3 fatty acids, found in foods including walnuts, some fruits and vegetables, and coldwater fish such as herring, mackerel, sturgeon, and anchovies.

“It not only plays a vital role in the health of the membrane of every cell in our body, it also helps protect us from a number of key health threats,” says Laurie Tansman, MS, RD, CDN, a nutritionist at Mount Sinai Medical Center in New York. Continue reading “Good Fat, Bad Fat: The Facts About Omega-3”

Vitamin C and Chest Pain

I found an interesting article about chest pain and Vitamin C. The theory is that heart disease is a form of mild scurvy brought on by a lack of Vitamin C or Ascorbate Acid. Humans, other primates and guinea pigs are unable to metabolize Ascorbate in their livers and thus need to take it in through diet or supplements.

Case Report: Lysine/Ascorbate-Related Amelioration of Angina Pectoris

Linus Pauling

Abstract 
It is gratifying to report the first observation of the amelioration of effort angina by the use of high-dose L-lysine and ascorbate in a man with severe coronary artery disease (CAD). This regimen was based on the hypothesis that, in thrombotic atherosclerosis, lipoprotein(a) [Lp(a)]‹ size-heterogeneous, LDL- like particles d displaying independent risk activity for CAD ‹initiates plaque formation by binding to fibrin in the damaged arterial wall. This postulated mechanism correlates with the findings that apoliprotein(a) [apo(a)] has a striking homology to plasminogen and the Lp(a) accumulates in atherosclerotic lesions in the arteries of man (Rath et al., 1989)and the hypoascorbic guinea pig (Rath and Pauling, 1990a, 1990b) and in occluded bypass venous grafts (Cushing et al., 1989). It is hoped that the remarkable outcome in this single case will motivate clinicians to examine the efficacy of lysine and ascorbate in additional cases of refractory angina. 

Coronary Heart Disease Case History 
In late April 1991, a biochemist National Science Medalist* with a familial trait of CAD told me that he experiences effort angina, in spite of medication and three coronary bypass operations. His father and a brother both died of CAD at age 62 he had his first angina attack at age 38. Now aged 71, this biochemist has fought CAD also by reducing risk factors (i.e., not smoking, exercising moderately, and diet/ weight control‹134 Ibs. at 5’5″). His first operation in 1978 (two vein grafts and one LIMA graft) precipitated a second operation (a parallel vein graft) five months later. Stripping of saphenous veins in the first operation induced massive swelling, thrombi, and infection in his leg; bilateral pulmonary emboli; and loss of patency in a vein graft. In 1987, following an attack of unstable angina, he was hospitalized for coronary angiography, adjustment of medications, and a Tl-stress test. A third operation in April 1990 followed attacks of unstable angina, a small MI, and angiography that revealed total occlusion of his right coronary artery and all bypass grafts except for a patent LIMA graft. Unfortunately, this LIMA was lacerated while freeing dense adhesions early in the third operation and required urgent heart-lung bypass cannulation and vein-patch repair; additionally, three venous grafts were made to left coronary arteries. The operation, which diminished but did not eliminate effort angina, left him with 1.8 liters of left-sided pleural effusate that was resistant to diuretics and tapping, and took 10 months to resorb. Medication with beta-receptor and calcium-channel blockers and lovastatin was reinstated; also, 325 mg of aspirin given initially was reduced to 81 mg following bilateral eye hemorrhages and adhesions that impair his peripheral vision. To this medication, he added 6 g of ascorbate (acid form), 60 mg CoQ-10; a multivitamin tablet with minerals; additional vitamins A, E and a B-complex; lecithin; and niacin, on advice of his cardiologist to try to raise his HDL level. Nevertheless, he still had to take nitroglycerin sublingually to suppress angina during a daily two mile walk and when working in his yard. This effort angina continued to worsen, imparting a feeling of impending doom that was reinforced by his cardiologist’s admonition during a check-up in March 1991 that a fifth angiographic test and a fourth bypass operation were no longer options. Also, the saphenous veins from his groin regions and legs had all been used for previous grafts. 

Effect of the Addition of Lysine 
In this predicament and with his history of restenosis, I suggested that he continue ascorbate and add 5 g of L-lysine daily (ca., six times the lysine derived from dietary protein) to try to mitigate the atherosclerotic acitivity of Lp(a). After reading the 1990 Rath and Pauling reports and their manuscript titled “Solution to the puzzle of human cardiovascular disease”, he began taking I g of lysine in early May 1991 and reached 5 g (in divided doses eight hours apart) by mid-June. In mid-July, his HDL was, as usual, a low 28 mg/dl. A low-normal 0.9 mg/dl blood creatinine indicated that lysine could be increased, if needed. He could now walk the same two miles and do yard work without angina pain and wrote, “the effect of the lysine borders on the miraculous”. By late August, he cut up a tree with a chain saw, and in early September started painting his house. By late September, possibly from over-exertion, he again began to have angina symptoms during his walks, but after stopping strenuous work and increasing lysine to 6 g [calculated to provide a peak 280,000 molar excess in the blood over his then 6 mg/dl of Lp(a) to help compensate for the relatively high dissociation constant of lysine-Lp(a)] these symptoms stopped entirely by mid-October. His blood creatinine was still a normal 1.2 mg/dl. He attributes his newfound wellbeing to the addition of lysine to his other medications and vitamins. His wife and friends comment on his renewed vigor. 

Discussion 
This severe case of restenosing CAD was a difficult challenge to try to ameliorate by the addition of lysine. While a positive effect was anticipated, lysine had not been tested for activity in inhibiting or reversing Lp(a)-laden atherosclerotic plaques in hypoascorbemic guinea pigs (Rath and Pauling, 1990b). However, it was known that Lp(a) binds to lysine-Sepharose, immobilized fibrin and fibrinogen (Harpel et al., 1989); and the epithelial-cell receptor for plasminogen ( Gonzalez-Gronow et al., 1989). This binding specificity correlates with the genetic linkage on chromosome six and striking homology of apo(a) and plasminogen‹highly conserved multiple kringle-four domains, a kringle-five domain, and a protease domain (McLean et al., 1987). Moreover, using the molecular evolutionary clock, the loss in primates of the ability to synthesize ascorbate (Zuckerkandl and Pauling, 1962; Rath and Pauling, 1990a) and acquisition of Lp(a) (Maeda et al., 1983) both appear to have occurred about 40 million years ago. These observations and the presence of Lp(a) in sclerotic arteries (Rath et al., 1989; Rath and Pauling, 1990b) and in venous grafts (Cushing et al., 1989) indicate that atherosclerosis may be initiated by excess binding of Lp(a) to fibrin in vascular wall clots, thus interfering with normal fibrinolysis by plasmin. This thrombogenic activity, which is postulated to reside in plasmin-homologous domains of Lp(a), may help to stabilize the damaged vascular wall, especially in ascorbate deficiency (Scanu, Lawn, and Berg, 1991; Rath and Pauling, 1990a). Once bound to fibrin, the LDL-like domain of Lp(a) could promote atheromas (Scanu, Lawn, and Berg, 1991). In this scenario, high-dosage lysine could inhibit or reverse plaque accretion by binding to Lp(a). Independently, lysine benefits the heart as a precursor with methionine in the synthesis of L-carnitine, the molecule that carries fat into mitochondria for the synthesis of adenosine triphosphate (ATP) bond energy needed for muscular and other cellular activities (Cederblad and Linstedt, 1976). While his intake of 60 mg of CoQ-10, also required for ATP synthesis, prior to the addition of lysine improved his sense of wellbeing, it did not suppress his angina. Ascorbate without lysine also did not ameliorate angina, but it is needed as an antioxidant to protect the vascular wall against peroxidative damage and in hydroxylation reactions both in the synthesis of carnitine and in the conversion of procollagen to collagen (hydroxylation of prolyl and Iysyl residues) (Myllyla et al., 1984) to strengthen the extracellular matrix of the wall. 
Whatever the pathomechanisms of atherosclerosis, the addition of lysine to medications and vitamins, including ascorbate, markedly suppressed angina pectoris in this intractable case of CAD. While a single case is anecdotal, it is hoped that its remarkable success will motivate clinicians to commence studies as soon as possible of the general applicability of lysine and ascorbate in relieving angina pectoris, so as to decrease greatly the amount of human suffering with less dependence on surgical intervention. 

Footnote (p. 144) *The biochemist patient made a major contribution to this report, but wishes anonymity. 

References 
1. Cederblad G and Linstedt S: Metabolism of labeled carnitine in the rat. Archives of Biochemistry and Biophysics 175:173-182, 1976. 
2. Cushing GL, Gaubatz JW, Nava ML, Burdick BJ, Bocan TMA, Guyton JR, Weilbaecher D, DeBakey ME, Lawrie GM and Morrisett JD: Quantitation and localization of lipoprotein(a) and B in coronary artery bypass vein grafts resected at re-operation. Arteriosclerosis 9:593-603, 1989. 
3. Gonzalez-Gronow M, Edelberg J M and Pizzo SV: Further characterization of the cellular plasminogen binding site: Evidence that plasminogen 2 and lipoprotein(a) compete for the same site. Biochemistry 28:2374-2377, 1989. 
4. Harpel PC, Gordon BR and Parker TS: Plasminogen catalyzes binding of lipoprotein(a) to immobilized fibrinogen and fibrin. Proc. Natl. Acad. Sci. USA 86:3847-3851, 1989. 
5. Maeda N, Bliska JB and Smithies O: Recombination and balanced chromosome polymorphism suggested by DNA sequences 5′ to the human deltaglobin gene. Proc. Natl. Acad. Sci. USA 80:5012-5016, 1983. 
6. McLean JW, Tomlinson JE, Kuang WJ et al.: cDNA sequence of human apolipoprotein(a) is homologous to plasminogen. Nature 330:132-137, 1987. 
7. Myllyla R, Majamaa K, Gunzler V, Hanuska-Abel HM and Kivirikko KI: Ascorbate is consumed stoichiometrically in the uncoupled reactions catalyzed by prolyl-4-hydroxylase and Iysyl hydroxylase. Journal of Biological Chemistry 259:5403-5405, 1984. 
8. Rath M, Niendorf A, Reblin T, Dietel M, Krebber HJ and Beisiegel U: Detection and quantification of lipoprotein(a) in the arterial wall of 107 coronary bypass patients. Arteriosclerosis 9:579-592, 1989. 
9. Rath M and Pauling L: Hypothesis: Lipoprotein(a) is a surrogate for ascorbate. Proc.. Natl. Acad. Sci. USA 87:6204-6207, 1990a. 
10. Rath M and Pauling L: Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. Proc. Natl. Acad. Sci. USA 87:9388-9390, 1990b. 
11. Scanu M, Lawn RM and Berg K: Lipoprotein(a) and atherosclerosis. Annals of Internal Medicine 115:209-218, 1991. 
12.Zuckerkandl E and Pauling L: Molecular disease, evolution, and genic heterogeneity. In: Horizons in Biochemistry, eds. Kasha M. and Pullman B. (Academic Press, New York) pp. 189-225, 196

[asa]B00008I8NJ[/asa]

[asa]B001G7QTKG[/asa]

Vitamin C may be a life-saver

Vitamin C may be a life-saver

Mega-doses of Vitamin C can counter avian flu, hepatitis and herpes, and can even control the advance of Aids

Read the original article at The Independent

By Jane Feinmann

Imagine that a deadly virus is sweeping the world, killing and maiming hundreds of thousands of children. Nothing seems able to stop it – until a doctor stands up at the American Medical Association and reports on 60 cases involving severely infected children, all of whom have been cured. Yet his work, subsequently reported in a peer-review journal, is ignored, leaving the virus to wreak havoc for decades.

Imagine that a deadly virus is sweeping the world, killing and maiming hundreds of thousands of children. Nothing seems able to stop it – until a doctor stands up at the American Medical Association and reports on 60 cases involving severely infected children, all of whom have been cured. Yet his work, subsequently reported in a peer-review journal, is ignored, leaving the virus to wreak havoc for decades.

This isn’t a docudrama about some futuristic plague – it’s a true story about what happened in June 1949 when polio was at its peak. Dr Frederick Klenner, a clinical researcher from Reidsville, North Carolina, reported that a massive intravenous dose of Vitamin C – up to 20,000mg daily for three days (today’s recommended daily allowance is 60mg) – had cured 60 of his patients. The findings were published in a medical journal, yet there was virtually no interest. Apart from a couple of minor trials, no attempt was made to find out if they had any scientific substance.

Relating this curious incident in a new book, Vitamin C, Infectious Diseases & Toxins: Curing the Incurable, Dr Thomas Levy, a US cardiologist, admits to being gripped by a range of emotions when he came across Klenner’s work and other studies that replicated it. “To know that polio had been easily cured yet so many people continued to die, or survived to be permanently crippled by it, was difficult to accept.”

Levy argues that the medical profession has routinely ignored research showing that high doses of Vitamin C can combat bacteria, toxins and severe viral infections including avian flu, SARS, hepatitis and herpes. And this is not a case of doctors sniffing at anecdotal evidence from a handful of enthusiasts. “Vitamin C is possibly the best-researched substance in the world. There are more than 24,000 papers and articles on the authoritative clinical website, Medline. Yet virtually the all the evidence has been dismissed.” Levy even claims that Aids can be controlled if a high enough dosage of Vitamin C is maintained.

This is not the first time doctors have had their cages rattled over the benefits of Vitamin C. The controversy has been simmering since 1753, when just a couple of sucks of a lime were shown to prevent scurvy. In the 1950s the chemist Linus Pauling, a double Nobel prize-winner, promoted the use of mega-doses of Vitamin C, but his research was rubbished by clinicians.

Recently, the anti-Vitamin C sentiment has grown. It has been blamed for causing the formation of kidney stones, and a study published in the journal Science in 2001 found that even 200mg doses of Vitamin C “facilitated the production of DNA-damaging agents associated with a variety of cancers”. This finding was widely interpreted as proving that Vitamin C causes cancer.

Britain’s Food Standards Agency recommends taking a maximum of 1,000mg of Vitamin C a day. But a directive going through the European Parliament aims to reduce this to less than 100mg in an attempt to harmonise dosages across the Continent. Despite being dubbed “illegal” by the advocate general of the European Court of Justice last week, the directive could still be passed.

The controversy has not put off consumers, many of whom take Vitamin C to ward off colds. The 1,000 mg capsule is the most popular single vitamin in Britain, with the 500mg version second.

Some people argue that we can get sufficient Vitamin C from a diet rich in fruit and vegetables, but Levy disagrees. The problem, he says, is that a genetic design fault makes us unable to synthesise our own Vitamin C. Levy claims that while recommended daily allowances of 60mg are enough to prevent the development of scurvy in otherwise healthy people, much higher levels are required to maintain health when an infection strikes. At such times, the body begins to “metabolise unusually large amounts of vitamin C, keeping stores so depleted that the recommended daily allowance will not even prevent many of the symptoms of scurvy from developing”.

Levy claims that the reason why most animals stay healthy throughout their lives, while humans spend years coping with one or more chronic diseases, is that animals make their own Vitamin C. The wild goat, for instance, makes around 13,000mg a day, rising to 100,000mg when faced with life-threatening infectious or toxic stress, according to a 1961 study published in the Annals of the New York Academy of Sciences.

So, is Levy right? Should everyone be taking mega-doses every day and having intravenous infusions when they fall ill? Possibly.

Dr Rodney Adeniyi-Jones regularly gives 20,000mg doses to people with arterial disease and as part of a flu treatment protocol, describing its effects as “beneficial… but not miraculous”. And Professor George Lewith of the Centre for Complementary and Integrated Medicine says that while Vitamin C is not a panacea, it does have clinical benefits depending on the dosage. “There may be doses that are therapeutic, while another dose may be damaging for the same condition. It is not a dose-response curve as with pharmaceuticals, and we need to be cautious until this is better understood.”

But he also warns that: “Many of the [Vitamin C] trials have been badly done and what evidence exists is mixed. Both those in favour and against high doses frequently misinterpret the data.”

Levy may well be seen to have an axe to grind, yet the evidence seems to support his view that apart from causing diarrhoea, mega-doses of Vitamin C are not toxic. He says that a series of studies published in leading journals have shown that, far from causing cancer, Vitamin C is a safe supplement for chronic cancer patients. Further large studies suggest that supplements do not put a normal person at greater risk of developing kidney stones.

According to Levy, the problem is not that people might take too much, but that they won’t take enough – and thus won’t get the desired effects. “There’s a popular medical view that taking Vitamin C just makes expensive urine. Some of it is lost in urine, but the more you consume, the more stays in your body.”

With a new book on the way claiming that Vitamin C deficiency is also a primary cause of cardiovascular disease, Levy cannot be accused of underselling his case. Nor can he overcome the fact that proper clinical trials are still desperately needed. Considering its overall safety, there appears to be no good reason why anyone with a chronic or acute health problem should not try, at the very least, a couple of week’s regime of two or three 1,000mg tablets of Vitamin C a day.

Need to Know: So how much should you take?

* For a cold

Three 1,000mg doses a day, according to the campaign group Consumers for Health Choice.

* For flu

Although it’s more serious, the viral load is similar, according to research, and taking up to 20,000mg a day could be beneficial.

* For shingles

Research has shown that this painful post-viral condition can be pretty well cured by an injection of 3,000mg of vitamin C. Taking four 1,000mg tablets orally for three days could be worthwhile as well.

* For a hangover

Taking 1,000mg daily in the week before a booze-up reduces stress on the liver. If you’re drunk and want to look sober, a large dose of vitamin C will prevent drunken behaviour, according to a 1986 study, “Alcohol and Alcoholism”.

* To maintain your health

A 1,000mg daily dose is regarded as safe by the Food Standards Agency, and adequate to keep sufficient vitamin C in the plasma and tissues. “We believe this is absolutely safe and definitely beneficial to people’s health,” says Sue Croft of Consumers for Health Choice.

Ketosis & Ketone Test Strips (Ketostix)

What are ketones?

Ketones are a normal and efficient source of fuel and energy for the human body. They are produced by the liver from fatty acids, which result from the breakdown of body fat in response to the absence of glucose/sugar. In a ketogenic diet, such as Atkins … or diets used for treating epilepsy in children, the tiny amounts of glucose required for some select functions can be met by consuming a minimum amount of carbs – or can be manufactured in the liver from PROTEIN. When your body is producing ketones, and using them for fuel, this is called “ketosis”.

How will ketosis help me to lose weight?

Most reducing diets restrict calorie intake, so you lose weight but some of that is fat and some of it is lean muscle tissue as well. Less muscle means slowed metabolism, which makes losing weight more difficult and gaining it back all too easy. Ketosis will help you to lose FAT. Continue reading “Ketosis & Ketone Test Strips (Ketostix)”

ECA Stack – Ephedrine, Caffeine and Aspirin – Thermogenic Effects

I am going to file this one under fad diets and throw in a word of caution. Ephedrine is a powerful drug and can have some serious side effects. Read and use this information at your own risk. I am posting this information because I’ve noticed a lot of my automatically generated Google adds are trying to lure you into buying different weight loss supplements and this is the only one with any sort of legitimate science to back it up.

I have used an ECA stack in the past but like Dumbo’s Feather (which if you remember helped him to fly) I think it had more of a placebo effect. Yes, I lost weight but I would attribute most of it to a good clean diet and an insane amount of grueling physical exercise. I am not advocating this method, nor am I using it myself. The FDA considered Ephedra dangerous enough to ban its sale as a supplement. It is still legal to buy over the counter for relief of asthma symptoms.  Anyway, on to how and why it works.

The following abstract is from an article by Nadir Yehya from the University of California, Los Angeles.

The field of obesity management is coming to appreciate the efficacy of pharmacological
treatments. For the past twenty years the thermogenic effects of sympathetic stimulation have been known and described. Recent studies have demonstrated that treating patients with a
drug combination including the sympathomimetic ephedrine, the stimulant caffeine, and the analgesic aspirin (ECA combination) will stimulate thermogenesis and result in lowered weight but maintained muscle mass. This protein-sparing lipolysis has been attributed to the elevated levels of cAMP generated by the ECA combination. In rat studies, the mechanism of action has been well characterized in vitro and although there is some discrepancy in humans, a similar mechanism seems to be active. Randomized placebo-controlled trials have demonstrated the short-term efficacy of the ECA combination, but long-term studies are lacking. Most studies have also demonstrated the incidence of short-term side effects associated with excessive sympathetic stimulation, and have shown them to be transient and mild. Future studies should focus on the long-term efficacy of the ECA combination, and the effects of stopping treatment on the maintenance of fat loss.

This research concludes that the ECA combination provides protein sparing lipolysis which translates to keeping muscle while burning fat. To lose wieght the body must break down and use fat. Typically, this catabolic activity burns both muscle and fat. Weight is lost but losing both fat and muscle is a bad thing. The ECA stack spares the protein or muscle in favor of fat.

So, the ECA stack burns fat and spares muscle. Let’s check the wiki to see how it works.

From a Wikipedia article:

The effects of the ECA stack in weight loss are primarily due to the ephedrine component. Ephedrine acts both as a beta agonist and stimulates the release of norepinephrine. Increased circulating norepinephrine in the body then acts on white adipose tissue by increasing cAMP levels. This causes a thermogenic effect, raising body temperature and increasing the user’s metabolism in conjunction with the rest of the stack.

However, the body’s negative feedback system then activates to normalize the metabolism. This is done via the production of phosphodiesterase inside the cells, and prostaglandins outside the cell, which both lower cAMP levels within the cell.

Caffeine inhibits the production of phosphodiesterase inside the cell and therefore slows cAMP breakdown. It also binds with and competitively inhibits adenosine receptors in the brain, triggering the release of epinephrine and increasing cAMP levels further.

Aspirin inhibits prostaglandin production outside of the cells, which, in conjunction with caffeine, greatly prolongs the thermogenic effects and increased metabolism by sustaining elevated cAMP levels.

Ephedrine also has an anorectic, or appetite-suppressing, effect. However, these effects only last for about two weeks if the stack is not cycled, as the body becomes tolerant to ephedrine to some degree. It is estimated that 60%–75% of the weight loss from using the ECA stack comes from the anorectic effect, and the remainder from thermogenesis.

The final component in weight loss of the ECA stack is that of a simple stimulant; the higher epinephrine and norepinephrine levels result in increased aerobic exercise performance and less fatigue.

Basically, the Ephedrine increases your metabolism and has a anorectic effect making you less hungry. The caffiene and asprin keep these effects going by blocking the body’s ability to compensate for these effects naturally.

Typically the ECA stack is consumed two or three times per day in a 1:10:10 or 1:10:15 ratio of ephedrine:caffeine:Aspirin. This translates to approximately 25 mg of ephedrine, 200 mg of caffeine and 325 mg of Aspirin for a single dose.

Once again, there are risks involved in taking this and it should be used with caution.