Aspirin and Heart Attacks
With all of the talk about nonsteroidal anti-inflammatory drugs (NSAIDs) increasing the risk of heart attack and stroke, it seems like there is a lot of advertising going on claiming that aspirin can reduce your risk of heart attack. Are these claims really credible, or just more pharmaceutical sales hype?
One of the most misleading commercials was from an aspirin manufacturer that was claiming that their product had been shown to reduce the risk of a second heart attack by 50%. Sounds really impressive until you look at how they came to their conclusion. It was revealed on news program that the company had started with around 100 test subjects. After being given the aspirin therapy for a length of time, the drug company chose only 6 participants to base their conclusion on. Out of the 6 participants, 3 had not had a second heart attack by that time. Thus the drug company came to the conclusion that their product reduced the risk of a second heart attack by 50%.
Numerous other companies have been making similar claims. And aspirin therapy is even been recommended to take during a heart attack. This is a widely accepted concept, and is even being recommended by some doctors. Though, this practice has never been proven safe, or beneficial in any way. In fact, the practice is being questioned by other doctors because evidence is contrary to this common belief.
Generally NSAIDs contract blood vessels and promote the formation of blood clots by inhibiting the hormone prostacyclin. Aspirin inhibits prostacyclin as well, leading to blood vessel constriction. Unlike other NSAIDs though, aspirin actually helps to prevent blood clots though by interfering with platelet clumping. Blood clots are well known for causing heart attacks and thrombic stroke. This is where the notion that aspirin would help prevent a heart attack, or reduce risk of death from a heart attack, got started. Aspirin does not dissolve existing blood clots though. If a person takes an aspirin after a heart attack from a blood clot (thrombus), the aspirin will not dissolve the blood clot to restore blood flow. Although, as with all NSAIDs, aspirin will cause the blood vessels to contract, further reducing blood flow. This is the last thing that a person having a heart attack or angina should do. It is a decreased blood flow to the heart that leads to angina, and an obstruction of blood flow that causes heart attacks in the first place.
Medical studies dating back to 1971 have consistently shown that aspirin does not benefit people during heart attacks. This claim is nothing more than sales propaganda. And some studies had to be stopped before results could be obtained due to the increased risk gastric hemorrhage and hemorrhagic stroke.
One aspirin study did appear at first to reduce the risk of death from heart attack. This study was conducted by two groups of doctors, one in England, and the other in the United States. The group of doctors in England took plain aspirin, and concluded no reduced risk of death from aspirin therapy. The U.S. group of doctors used aspirin buffered with magnesium. This group found a slight benefit from the therapy. The benefit was not from the aspirin though. Instead, the benefit resulted from the magnesium added to the aspirin. Magnesium is a well known for relaxing blood vessels. By relaxing the blood vessels, magnesium actually increases blood flow to the heart, opposite of aspirin’s effect.
Hemorrhage is the most dangerous side effect of aspirin therapy. If a bleed starts due to a ruptured blood vessel, the inability to clot can have devastating consequences. For example, NSAIDs kill over 16,000 people a year. Nearly all of these deaths are due to internal bleeding disorders. These bleeding disorders are primarily gastric bleeds and hemorrhagic strokes. This increased risk of bleeds is not only due to the blood thinning effects of the aspirin, but also from the blood vessel weakening effects of the drug, which increases the likelihood that a blood vessels will rupture.
My grandfather actually lost his eyesight completely in one eye from taking aspirin. He developed a bleed in the eye from a ruptured blood vessel, which was likely weakened by the aspirin therapy. Because the aspirin had also thinned out his blood so much, the bleed could not clot as it would normally do, and he went blind in that eye.
There is also a problem with the constant claims of aspirin reducing the risk of a second heart attack or stroke by a certain percentage, which is often done by these drug companies. Both heart attacks and strokes are unpredictable. So how can they claim that aspirin prevented a second heart attack, or stroke, when it is impossible to tell if the person would have had a second heart attack or stroke if they had not taken the aspirin? And what if all the people in the study were to have a second heart attack or stroke the day after the study is completed? The percentage would still remain the same since the heart attacks or strokes occurred outside the study timeframe. These are just a few examples of how drug studies are manipulated to make drugs appear safe or effective.
NSAIDs and the Heart
The nonsteroidal anti-inflammatory drugs (NSAIDs) Celebrex and Vioxx have recently come under fire when it was admitted that these drugs could significantly increase the risk of heart attack and stroke. Are these the only NSAIDs capable of increasing this risk though?
Many heart disturbances, including heart attack, result from decreased blood flow to the heart. Common causes of decreased blood flow include arterial plaque formation, blood clots, and narrowing of the arteries from muscular contraction of the blood vessels.
Arterial plaque formation starts with damage to the blood vessel walls. This leads to depositing of cholesterol and calcium on the arterial walls. One of the most common causes of the arterial damage is high blood pressure caused from constriction of blood vessels. Various factors may lead to blood vessel constriction. These include elevated serum calcium, elevated insulin levels in type 2 diabetes, and epinephrine (adrenaline) induced constriction. NSAIDs constrict blood vessels as well, which leads to an elevation of blood pressure. Increased blood pressure may result in narrowing of the arteries from plaque due to resulting arterial damage. This narrowing of the arteries not only increases the risk of heart attack, but also of thrombic and embolytic stroke.
Because NSAIDs constrict blood vessels, these drugs increase the risk of angina, heart arrhythmias, and heart attack in people with already impaired perfusion to the heart. These include individuals with previous angina, or heart attacks, history of congestive heart failure, diabetics, and individuals who tend to put out too much epinephrine, etc.
Further risk comes from the fact that NSAIDs inhibit prostaglandins, including prostacyclin, also known as prostaglandin I2 (PGI2). PGI2 is produced by healthy endothelial cells of blood vessels. The roles of PGI2 are to dilate blood vessels, to increase blood flow, and to inhibit platelet formation and blood clot formation. By dilating blood vessels, blood pressure is reduced, and more blood reaches critical areas, such as the brain and heart. This also lowers the risk of heart disease by reducing arterial damage, which would otherwise lead to plaque formation. By reducing blood clot formation, the risk of heart attack and thrombic stroke are reduced. Both damage to endothelial cells and the use of NSAIDs inhibit PGI2 production, which increases blood clot formation and reduces blood flow. Production of blood clots and reduction of blood flow increase the risk of angina, arrhythmias, and heart attack, as well as transient ishemic attacks, and thrombic stroke.
As we can see, the increased risk of heart attack and stroke are not limited to certain NSAIDs, but rather can occur with all pharmaceutical NSAIDs. And the problem is not a new finding. The blood vessel constricting effects of NSAIDs have been known for decades. Part of the drug approval process includes knowing how the drug works. NSAIDs are known, and have been known, to work by consticting blood vessels. When blood vessels are overdilated by inflamamtory prostaglandins, they become permeable, which leads to leakage of fluids in to the surounding tissues, and resulting inflammation. By consticting blood vessels, NSAIDs prevent blood vessels from leaking. It is well known that the adverse effects of liver and kidney failure by NSAIDs is due to impeded blood flow to these organs due to this constiction of the blood vessels. Other organs, such as the heart, as well as glands are adversely affected by the impeded blood flow in the same manner. Therefore, the only explanation for the increased risk of heart attack and stroke being “discovered” recently would be that the drug companies and FDA knew about the problem all along and just recently decided to make this known fact public.
NSAIDs Part 1
The nonsteroidal anti-inflammatory drugs (NSAIDs) Celebrex and Vioxx have recently come under fire when it was admitted that these drugs could significantly increase the risk of heart attack and stroke. Are these the only NSAIDs capable of increasing this risk though?
Many heart disturbances, including heart attack, result from decreased blood flow to the heart. Common causes of decreased blood flow include arterial plaque formation, blood clots, and narrowing of the arteries from muscular contraction of the blood vessels.
Arterial plaque formation starts with damage to the blood vessel walls. This leads to depositing of cholesterol and calcium on the arterial walls. One of the most common causes of the arterial damage is high blood pressure caused from constriction of blood vessels. Various factors may lead to blood vessel constriction. These include elevated serum calcium, elevated insulin levels in type 2 diabetes, and epinephrine (adrenaline) induced constriction. NSAIDs constrict blood vessels as well, which leads to an elevation of blood pressure. Increased blood pressure may result in narrowing of the arteries from plaque due to resulting arterial damage. This narrowing of the arteries not only increases the risk of heart attack, but also of thrombic and embolytic stroke.
Because NSAIDs constrict blood vessels, these drugs increase the risk of angina, heart arrhythmias, and heart attack in people with already impaired perfusion to the heart. These include individuals with previous angina, or heart attacks, history of congestive heart failure, diabetics, and individuals who tend to put out too much epinephrine, etc.
Further risk comes from the fact that NSAIDs inhibit prostaglandins, including prostacyclin, also known as prostaglandin I2 (PGI2). PGI2 is produced by healthy endothelial cells of blood vessels. The roles of PGI2 are to dilate blood vessels, to increase blood flow, and to inhibit platelet formation and blood clot formation. By dilating blood vessels, blood pressure is reduced, and more blood reaches critical areas, such as the brain and heart. This also lowers the risk of heart disease by reducing arterial damage, which would otherwise lead to plaque formation. By reducing blood clot formation, the risk of heart attack and thrombic stroke are reduced. Both damage to endothelial cells and the use of NSAIDs inhibit PGI2 production, which increases blood clot formation and reduces blood flow. Production of blood clots and reduction of blood flow increase the risk of angina, arrhythmias, and heart attack, as well as transient ishemic attacks, and thrombic stroke.
As we can see, the increased risk of heart attack and stroke are not limited to certain NSAIDs, but rather can occur with all pharmaceutical NSAIDs. And the problem is not a new finding. The blood vessel constricting effects of NSAIDs have been known for decades. Part of the drug approval process includes knowing how the drug works. NSAIDs are known, and have been known, to work by consticting blood vessels. When blood vessels are overdilated by inflamamtory prostaglandins, they become permeable, which leads to leakage of fluids in to the surounding tissues, and resulting inflammation. By consticting blood vessels, NSAIDs prevent blood vessels from leaking. It is well known that the adverse effects of liver and kidney failure by NSAIDs is due to impeded blood flow to these organs due to this constiction of the blood vessels. Other organs, such as the heart, as well as glands are adversely affected by the impeded blood flow in the same manner. Therefore, the only explanation for the increased risk of heart attack and stroke being “discovered” recently would be that the drug companies and FDA knew about the problem all along and just recently decided to make this known fact public.
NSAIDs Part 2
Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used as pain relievers for inflammatory conditions. These drugs include ibuprofen (Advil, Motrin, Nuprin), naproxen, (Aleve), aspirin, rofecoxib (Vioxx), and celecoxib (Celebrex). Although, the pain relieving effects come with some potentially dangerous, and possibly deadly side effects.
NSAIDs work by inhibiting hormones, known as prostaglandins. Prostaglandins serve numerous functions within the body including regulating blood pressure, antidepressant, protecting the stomach from acid, etc. Inflammatory prostaglandins are essential for increasing blood flow to injured areas, which promotes healing by increasing oxygen and nutrient levels to the injured site. Prostaglandins do this by dilating the blood vessels. The inflammation occurs when the blood vessels are dilated, which causes the blood vessels to become permeable. This permeability causes the small blood vessels to leak fluid in to the surrounding tissues, which leads to the swelling. NSAIDs decrease the pain and swelling by countering these inflammatory prostaglandins. This causes the blood vessels to constrict, thereby reducing leakage of capillaries.
By reducing blood flow, NSAIDs actually inhibit the healing process. Although this is one of the more mild side effects of these drugs. Other side effects of NSAIDs include, but are not limited to, liver failure, kidney failure, aseptic meningitis, loss of vision, tinnitus (ringing in the ears), high blood pressure, depression, and bleeding ulcers.
The most common side effect is bleeding ulcers, which leads to the majority of the over 16,000 deaths annually from these drugs. These ulcerations occur from the inhibition of another prostaglandin required to form the protective mucous lining of the stomach. This mucous coating protects the stomach wall from stomach acid. By inhibiting the formation of the protective stomach lining, the stomach wall is prone to direct attack from the stomach acid, leading to ulceration of the stomach wall and internal bleeding.
Constriction of blood flow leads to elevation of blood pressure. Loss of vision and tinnitus occur from reduced blood flow to the eye and in the area of the neck, due to the blood vessel constriction.
Prostaglandins play a major role in mood. By countering prostaglandins, the use of NSAIDs will cause depression.
Kidney and liver failure occur from a lack of blood flow to these organs. In fact, 2 dozen people died from ibuprofen induced hepatitis during clinical trials. People with poor perfusion to the organs, such as those with congestive heart failure, diabetes, Raynaud’s, etc. are at a higher risk for the damage or organ failure since blood flow is already reduced in these individuals. Further constriction of the blood vessels by NSAIDs may completely cut off the blood supply to organs and glands leading to damage or complete failure.
Contrary to popular belief, it does not take long term use or overdose to cause organ failure. In fact a single, recommended, dose can cause sufficient constriction of the blood vessels to cause damage. I know of 4 people that developed kidney failure after taking a single recommended dose of ibuprofen. And the number of cases is most likely heavily underreported since adverse effects of drugs are commonly attributed to other disorders.
The NSAID Bextra, manufactured by the pharmaceutical company Pfizer, was approved by the FDA in November of 2001. Bextra was later recalled after it was revealed that the drug could cause potentially deadly allergic reactions, and the disorders Steven’s-Johnson syndrome, and toxic epidermal necrolysis.
The new proposals for warning labels on these drugs need to include the risk of adverse effects from recommended use as well. Not only long term use and overdose as is currently being recommended.
A few other recommendations that I feel should be implemented include:
Pulling NSAIDs off the market as was done with Bextra since the safety studies were either never done, or were suppressed by the drug companies, or ignored by the FDA, to get approval.
Requiring more evidence of safety before approving these drugs.
Charging pharmaceutical drug company executives, and FDA officials, with manslaughter when it is shown that side effects were hidden to gain approval, and it has resulted in deaths. Right now only pharmaceutical companies are held liable. Although only by civil liability, not criminal. Fines are sometimes imposed against pharmaceutical companies, although they are hardly punishment. Fines are generally around a million dollars, or slightly higher when the drug companies have made hundreds of millions or even billons of dollars in profits. This is hardly punishment, and encourages the drug companies to hide adverse effects since profits will far outweigh any liabilities.
Heavier civil penalties against the drug companies to actually punish them for deliberately hiding known side effects, and for manipulating research to make their drugs appear safe and effective
Civil lawsuits should not only include the drug companies, but also the FDA officials who receive gifts, payoffs, and jobs to push the drugs through the approval process.
Cracking down on illegal investments by FDA officials in to the drug companies they regulate. This is a violation of insider trading laws. Despite this, nothing has been done to correct this illegal activity within the FDA despite the illegal investments being reported for nearly 3 decades.
Faster action on pulling drugs from the market suspected of causing harm until safety of the drugs can be established.
Testing of drugs by independent testing agencies. Currently the FDA requires the drug companies to provide their own safety data to obtain approval. If the drug company has already invested millions of dollars in to the drug, and a safety issue appears the drug company is not going to reveal the safety issue and risk approval being denied. This is a major reason drugs are being approved, then being pulled several years later, after the drug companies have not only paid for the cost of approval, but have also paid stockholders and made millions of dollars or more in profits.
Drugs requiring a prescription when they are originally approved should remain only available by prescription. They should not be made available over the counter when the drug’s patent expires. The chemistry, or dangers, of the drug do not change just because the patent has expired on the drug.
Decline in Breast Cancer
The incidence of breast cancer has declined 7% in the past few years. The big question is why?
The most likely explanation is declining use of estrogen replacement therapy (ERT) by women. Researchers have shown that the decline in breast cancer rates started as soon as it was publicly admitted that ERT had been shown to increase the risk of breast cancer. When this long held knowledge was made public, many women immediately went off their hormone replacement therapies.
Even though this is strong evidence that ERT was directly increasing breast cancer rates, other researchers are trying to argue against the evidence. One claim was made that the decrease in breast cancer rates may be due to better mammography techniques. Actually, if better mammography techniques were being implemented, then the incidence of breast cancer would be going up, not down. Standard mammography systems can miss malignant tumors, especially if they are small. Utilizing more advanced mammography techniques would allow for the detection of smaller tumors that would otherwise be missed. Because more tumors would be detected, the incidence of breast cancer would actually go up.
The increased risk of breast cancer from ERT has been well known for decades by the medical community. It has only been in the past few years that this increased risk has been widely reported in the media though. Other adverse effects of ERT, including hypothyroidism, increased risk of heart attack and strokes from blood clots, weight gain, depression, and other adverse effects still do not get the media’s attention.
Premarin is the most widely used drug for ERT. The name Premarin comes from its source, which is pregnant mare’s urine (PREgnant MARe’s urINe). Premarin is on average 3,000 times stronger than the estrogens produced by the human body. It is well known that human estrogens may cause or promote breast cancers in women, as well as other disorders. So why would the medical establishment try to convince women that something 3,000 times stronger than their own estrogens is essentially safe over the last three decades?
And why would the medical establishment tell women to take Premarin to reduce the risk of heart disease when estrogen is well known to cause blood clots? Blood clots are a common cause of heart attacks, and strokes.
The only real benefit of ERT that I see is the protective effect on bones. Estrogens do not promote bone growth. Instead they can help prevent bone loss after natural, or surgically induced, menopause. Although, it requires much more than estrogen to prevent osteoporosis, and there are safer alternatives. For example, the mineral boron has been shown in clinical studies to prevent bone loss in the absence of ERT at a daily dosage of 3mg.
Vitamin C Functions
The most popular supplement ever is obviously vitamin C. This antioxidant serves the body in so many ways.
As a water-soluble antioxidant, vitamin C helps protect the inside of cells from free radical damage. A synthetic, oil soluble form, a vitamin C is also available. The oil soluble form can help protect the cell membrane.
Vitamin C is essential for the synthesis of collagen and elastin. These proteins give strength and elasticity to the skin, hair, nails, bones, cartilage, tendons, ligaments, arterial walls, and other tissues. Deficiencies of these proteins lead to wrinkles, emphysema, diverticulitis, osteoporosis, osteoarthritis, and other disorders.
The immune system is dependent on vitamin C for the production of antibodies, interferons, immune enzymes, and immune cells. The thymus gland, considered the master gland of immunity, and the adrenal glands, which also play a major role in the immune system, are both highly dependent on vitamin C for proper function. In fact, the adrenal glands receive priority of vitamin C over the rest of the body.
The primary cause for vitamin C deficiencies is stress, including pain. Stress causes the adrenal glands to work overtime, increasing the requirement for vitamin C by the adrenal glands. Because the adrenal glands receive priority of vitamin C over the rest the body, this reduces available levels to other parts of the body. Stimulants, such as caffeine and nicotine, also overwork the adrenal glands reducing vitamin C levels in the body.
Synthetic Vitamin C
Many people assume that any product sold in a health food store is natural. Actually, most of the vitamins and minerals, as well as hormone products, and other items are synthesized in a lab. This includes the majority of vitamin C products sold in health food stores.
Natural vitamin C is too costly to extract, therefore the majority of vitamin C is synthesized from sugars, most often from corn. This includes products, such as palm C, which sounds natural. Palm C is synthesized from palm sugar though.
Synthetic vitamin C’s will be listed on the bottle as ascorbic acid. Natural bioflavonoids are frequently added because they aid in the function of vitamin C. Bioflavonoids occur naturally in natural sources of vitamin C, such as berries.
Some companies buffer the acidity of the ascorbic acid with minerals. Examples are calcium, sodium, and magnesium ascorbates. These are beneficial for people who cannot tolerate the acidity of the ascorbic acid. Although, I generally prefer non buffered forms of vitamin C. The majority of people have insufficient levels of stomach acid to digest and absorb nutrients. Non buffered vitamin C increases stomach acidity, aiding in digestion and absorption, when taken with meals.
Synthetic vitamin C is extremely unstable, and quickly decomposes when exposed to light, heat, or moisture. Therefore, synthetic vitamin C should be kept in a cool, dry, dark place. I do not recommend storing bottles of vitamin C in a refrigerator though. Doing so can cause moist air to condense inside the bottle, making a wet mess, and destroying the vitamin C. Storing the vitamin C in a pantry would be a better choice.
Natural Vitamin C
I really prefer natural products whenever possible. Nature knows how to maintain a balance that we don’t see with synthetics. For example, the blood thinning coumarins and alfalfa are balanced by the blood clotting vitamin K. The coffee bean, which contains the stimulant caffeine, is coated with a fleshy coating before processing that contains a sedative. The upper portion of the ephedra plant is a stimulant, while the roots are a sedative. Green tea contains a small amount of the stimulant caffeine, and the sedative amino acid theanine.
Vitamin C is another example. Natural vitamin C sources have several advantages over synthetic sources. For example, natural sources of vitamin C also contain synergistic bioflavonoids that must be added to synthetic C. Natural sources of vitamin C also contain compounds that help prevent deterioration of the vitamin C, which again is not true of synthetic vitamin C.
My favorite source of vitamin C is actually amla berry, also known as Indian gooseberry. The vitamin C in amla berry is actually 12 times stronger than synthetic vitamin C. Polyphenols in amla protect the vitamin C from oxidation, making it extremely stable. Additional advantages of amla include antiviral, antibacterial, antifungal, and anti-inflammatory effects. Amla protect the DNA from heavy metal damage, and significantly raises intracellular levels super oxide dismutase (SOD). SOD is an antioxidant, anti-inflammatory, and immune stimulatory enzyme.
My second choice for a natural vitamin C source is camu camu. Camu camu is native to South America. It is considered the highest plant source of vitamin C in the world. Camu camu does have one disadvantage though. Camu camu does not have the stability of amla, or acerola cherry.
My third choice is acerola cherry. This plant is thought to have originated from the Yucatan. Studies have shown widely varying rates of vitamin C, from lower than amla to higher than camu camu. As with amla berry, the vitamin C in acerola cherry is stabilized by polyphenols.
Other advantages of natural vitamin C sources are the fact that they are also sources of other vitamins. They also provide amino acids, minerals, and other nutrients that synthetic vitamin C does not offer.
Safety of Megadosing Vitamin C Part 1
It is the common belief that if a little is good, then more must be better. Although, many substances that provide beneficial effects to the body can be harmful, or even deadly, in large amounts. Even water or oxygen can be harmful or deadly in high amounts, or in the right circumstances.
Megadosing of vitamin C is a relatively common practice, especially among cancer patients. The belief is that large amounts of vitamin C can boost the immune system, and protect the body from free radical damage safely because the excess vitamin C will be eliminated from the body. How much of this is true though, and are there any risks?
Vitamin C does boost the immune system, and in does protect the body from some free radical damage. And it is true that excess vitamin C can be eliminated from the body. The practice of vitamin C megadosing does present some safety issues.
A severe deficiency of vitamin C can lead to a disease known as scurvy. Symptoms of scurvy include connective tissue breakdown, causing bleeding, muscle weakness, impaired wound healing, and nervous system disorders. It is believed that megadosing of vitamin C for extended periods of time, then drastically reducing the dose or going off cold turkey may lead to a condition known as rebound scurvy. Rebound scurvy is believed to occur when the body continues to excrete large amounts of vitamin C when megadoses are no longer being supplemented. Although, very few cases of rebound scurvy have been reported, and information about the cases have not been well-documented.
Safety of Megadosing Vitamin C part 2
Vitamin C is a water soluble compound, which can be easily flushed from the body. Although, vitamin C is a relatively unstable compound, and a portion of excess ingested vitamin C breaks down into oxalic acid in the body.
Oxalic acid is beneficial to the body as well as detrimental. As vitamin C breaks down in to oxalic acid, the oxalic acid actually serves as an antioxidant to the vitamin C helping to prevent oxidative destruction of the vitamin C. On the other hand, oxalic acid can bind with minerals forming insoluble oxalates. Of particular importance is calcium oxalate, which can form kidney stones. Studies have shown that oxalic stones, which make up 80% of kidney stones, only formed in people with kidney diseases, but not in healthy individuals at doses of 200mg daily. At 1,500mg daily intake there was only a tiny rise in the incidence of oxalic stone formation. It is believed that the insignificant rise is due to the fact that vitamin C is poorly absorbed by the body. Therefore, the higher levels of vitamin C are not being absorbed, and therefore are not converted in to oxalic acid.
Oxalic acid also binds with the electrolytes sodium and potassium, and the mineral magnesium. Among other functions of sodium and potassium is the regulation of heart rate. Magnesium serves a multitude of important functions including maintaining normal blood pressure, proper muscle function; including the heart, preventing muscle cramping, and insulin production.
Oxalic acid is an irritant to the urinary tract. Irritation of the urinary tract from oxalic acid can lead to urinary tract infections in sensitive individuals.
There is also concern that vitamin C may cause uric acid stones to form from excess excretion of uric acid. Acidification of the urine with vitamin C increases the ratio of uric acid to the more soluble sodium urate. For this reason, treatment of uric acid stones includes alkalinizing the urine with sodium bicarbonate (baking soda) or calcium citrate to increase sodium urate formation.
Excessive levels of vitamin C are contradicted in people suffering from kidney stones, gout, cirrhosis, kidney diseases, and certain other disorders.
Safety studies at doses of 200 to 1,500mg daily are conflicting. Safety studies of extremely high doses, up to 20,000 have not been done. Therefore I recommend not exceeding 2,000mg daily for healthy individuals. Normally, I recommend 500mg 3 times daily for most individuals. Slightly higher levels are recommended for smokers, individuals under a lot of stress, stimulant users; including caffeine (coffee, tea, guarana, kola nut, etc.), and those taking medications known to deplete vitamin C, such as Prednisone.
